Ovulation is known to damage fallopian tube epithelial (FTE) cells, promote cellular transformation, and contribute to the development of high-grade serous ovarian carcinoma (HGSC). While ovulatory follicular fluid–derived extracellular vesicles (EVs) have been shown to possess cell-transforming activity, it remains unclear whether these EVs persist in the peritoneal cavity after ovulation, potentially prolonging their exposure and enhancing their transformative effects on fallopian tube epithelial (FTE) cells. In this study, we collected follicular fluid (FF) and peritoneal fluid (PF) from women before and after ovulation, and investigated the oncogenic potential of ovulation-derived EVs on FTE cells using an anchorage-independent colony growth assay. We found that post-ovulatory PF exhibits significantly higher cell transformation activity compared to pre-ovulatory PF. This heightened activity correlates with an increased concentration of EVs and protein content in post-ovulatory PF. FF samples obtained from different ovulatory follicles of the same patient demonstrated consistent transformation activity, and FF- or post-ovulatory PF derived EVs retained this transforming capacity across FTE cells at varying stages of transformation. Our study reveals a novel mechanism by which ovulation may contribute to FTE transformation through the persistent oncogenic effects of EVs released into the peritoneal microenvironment. This finding provides new perspectives and directions for future cancer prevention, treatment, and potential diagnostic biomarker research.
{"title":"Ovulation-derived extracellular vesicles exhibit sustained oncogenic influence on the exposed fallopian tube fimbrial cells after drainage into peritoneal cavity","authors":"Aye Aye Khine , Pao-Chu Chen , Ying-Hsi Chen , Hsuan-Shun Huang , Tang-Yuan Chu","doi":"10.1016/j.tice.2026.103327","DOIUrl":"10.1016/j.tice.2026.103327","url":null,"abstract":"<div><div>Ovulation is known to damage fallopian tube epithelial (FTE) cells, promote cellular transformation, and contribute to the development of high-grade serous ovarian carcinoma (HGSC). While ovulatory follicular fluid–derived extracellular vesicles (EVs) have been shown to possess cell-transforming activity, it remains unclear whether these EVs persist in the peritoneal cavity after ovulation, potentially prolonging their exposure and enhancing their transformative effects on fallopian tube epithelial (FTE) cells. In this study, we collected follicular fluid (FF) and peritoneal fluid (PF) from women before and after ovulation, and investigated the oncogenic potential of ovulation-derived EVs on FTE cells using an anchorage-independent colony growth assay. We found that post-ovulatory PF exhibits significantly higher cell transformation activity compared to pre-ovulatory PF. This heightened activity correlates with an increased concentration of EVs and protein content in post-ovulatory PF. FF samples obtained from different ovulatory follicles of the same patient demonstrated consistent transformation activity, and FF- or post-ovulatory PF derived EVs retained this transforming capacity across FTE cells at varying stages of transformation. Our study reveals a novel mechanism by which ovulation may contribute to FTE transformation through the persistent oncogenic effects of EVs released into the peritoneal microenvironment. This finding provides new perspectives and directions for future cancer prevention, treatment, and potential diagnostic biomarker research.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"99 ","pages":"Article 103327"},"PeriodicalIF":2.5,"publicationDate":"2026-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145975975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-09DOI: 10.1016/j.tice.2026.103317
Domenico Ribatti
The vasculature surrounding tumors is not only a transport channel for nutrients, oxygen, and metabolites, but also a pathway for metastasis. This article summarizes the tissue and cellular origin of tumor endothelial cells, analyzes their characteristics, and summarizes their role in tumor progression and metastasis. Due to their distinct characteristics, tumor endothelial cells are a target for anti-angiogenic therapies, which aim to stop tumor blood vessel formation. Emerging therapeutic strategies aim at modulating both tumor endothelial cells and immune cells, not only to block angiogenesis but also to enhance the recruitment and activation of effector cells within the tumor.
{"title":"Tumor endothelial cells revisited: Their crucial role in tumor progression","authors":"Domenico Ribatti","doi":"10.1016/j.tice.2026.103317","DOIUrl":"10.1016/j.tice.2026.103317","url":null,"abstract":"<div><div>The vasculature surrounding tumors is not only a transport channel for nutrients, oxygen, and metabolites, but also a pathway for metastasis. This article summarizes the tissue and cellular origin of tumor endothelial cells, analyzes their characteristics, and summarizes their role in tumor progression and metastasis. Due to their distinct characteristics, tumor endothelial cells are a target for anti-angiogenic therapies, which aim to stop tumor blood vessel formation. Emerging therapeutic strategies aim at modulating both tumor endothelial cells and immune cells, not only to block angiogenesis but also to enhance the recruitment and activation of effector cells within the tumor.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"99 ","pages":"Article 103317"},"PeriodicalIF":2.5,"publicationDate":"2026-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145967307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-09DOI: 10.1016/j.tice.2026.103324
Zuping Wu , Ying Wang , Na Wu, Mingcheng Lu, Jiejun Shi
Neprilysin (NEP) is a membrane-bound endopeptidase that degrades various substrates, including natriuretic peptide, bradykinin, and substance P. It is distributed in various organs such as the heart, kidneys, and brain, regulating multiple physiological processes. This paper elucidates the role of NEP in osteogenic, chondrogenic, and myogenic differentiation processes, along with its time-specific expression during differentiation. We focus on how NEP regulates key pathways in skeletal muscle disorders, explores potential mechanisms, and demonstrates clinical symptom improvement. NEP degrades pro-inflammatory neuropeptides, thereby reducing local inflammation. Furthermore, NEP has been demonstrated to be responsible for the degradation of endogenous opioids, thus contributing to the regulation of pain. In the repair of skeletal muscle injury, NEP promotes the osteogenic, chondrogenic and myogenic differentiation of mesenchymal stem cells in animals, and achieves tissue regeneration. By discussing the therapeutic effect of NEP inhibitors and activators approved in clinic on skeletal muscle diseases, it was found that Shakubitril, a NEP inhibitor, promotes the thickening of cartilage growth plates and bone growth in animal models of chondrodysplasia. NEP activators promote muscle growth in castrated rats, rather than NEP inhibitor. This review emphasized the role of NEP in skeletal muscle growth and development, the changes in its levels in different skeletal muscle diseases, and its impact on disease progression. Finally, the efficacy of NEP related drugs in skeletal muscle diseases was discussed, hoping to provide a new way for the treatment of skeletal muscle diseases.
{"title":"The role of neprilysin in musculoskeletal diseases","authors":"Zuping Wu , Ying Wang , Na Wu, Mingcheng Lu, Jiejun Shi","doi":"10.1016/j.tice.2026.103324","DOIUrl":"10.1016/j.tice.2026.103324","url":null,"abstract":"<div><div>Neprilysin (NEP) is a membrane-bound endopeptidase that degrades various substrates, including natriuretic peptide, bradykinin, and substance P. It is distributed in various organs such as the heart, kidneys, and brain, regulating multiple physiological processes. This paper elucidates the role of NEP in osteogenic, chondrogenic, and myogenic differentiation processes, along with its time-specific expression during differentiation. We focus on how NEP regulates key pathways in skeletal muscle disorders, explores potential mechanisms, and demonstrates clinical symptom improvement. NEP degrades pro-inflammatory neuropeptides, thereby reducing local inflammation. Furthermore, NEP has been demonstrated to be responsible for the degradation of endogenous opioids, thus contributing to the regulation of pain. In the repair of skeletal muscle injury, NEP promotes the osteogenic, chondrogenic and myogenic differentiation of mesenchymal stem cells in animals, and achieves tissue regeneration. By discussing the therapeutic effect of NEP inhibitors and activators approved in clinic on skeletal muscle diseases, it was found that Shakubitril, a NEP inhibitor, promotes the thickening of cartilage growth plates and bone growth in animal models of chondrodysplasia. NEP activators promote muscle growth in castrated rats, rather than NEP inhibitor. This review emphasized the role of NEP in skeletal muscle growth and development, the changes in its levels in different skeletal muscle diseases, and its impact on disease progression. Finally, the efficacy of NEP related drugs in skeletal muscle diseases was discussed, hoping to provide a new way for the treatment of skeletal muscle diseases.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"99 ","pages":"Article 103324"},"PeriodicalIF":2.5,"publicationDate":"2026-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145967230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-09DOI: 10.1016/j.tice.2026.103321
Min Chen, Jialin Yao, Zuoli Liu
Renal fibrosis, a major pathological alteration in chronic kidney disease, is characterized by several changes, such as excessive extracellular matrix deposition, renal tubular cells' epithelial-mesenchymal transition, and fibroblast proliferation and activation. It has been demonstrated that rhubarb, a possible natural substance, may be used as a regular or supplemental treatment for chronic renal disease. Through a variety of pharmacological actions, including the anti-inflammatory and antioxidant qualities of natural ingredients, it may target renal fibrosis and produce its effects. This article offers fresh concepts for the creation of novel anti-renal fibrosis medications by succinctly introducing the pathological process of renal fibrosis and methodically summarizing the most recent studies on the use of rhubarb's natural constituents to treat renal fibrosis.
{"title":"Research on rhubarb's natural components and their potential for treating chronic kidney disease","authors":"Min Chen, Jialin Yao, Zuoli Liu","doi":"10.1016/j.tice.2026.103321","DOIUrl":"10.1016/j.tice.2026.103321","url":null,"abstract":"<div><div>Renal fibrosis, a major pathological alteration in chronic kidney disease, is characterized by several changes, such as excessive extracellular matrix deposition, renal tubular cells' epithelial-mesenchymal transition, and fibroblast proliferation and activation. It has been demonstrated that rhubarb, a possible natural substance, may be used as a regular or supplemental treatment for chronic renal disease. Through a variety of pharmacological actions, including the anti-inflammatory and antioxidant qualities of natural ingredients, it may target renal fibrosis and produce its effects. This article offers fresh concepts for the creation of novel anti-renal fibrosis medications by succinctly introducing the pathological process of renal fibrosis and methodically summarizing the most recent studies on the use of rhubarb's natural constituents to treat renal fibrosis.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"99 ","pages":"Article 103321"},"PeriodicalIF":2.5,"publicationDate":"2026-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145938893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-09DOI: 10.1016/j.tice.2026.103323
Linjie Lou , Ren Ye , Yisheng Huang
Background
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a key manifestation of metabolic syndrome in the liver. Its core pathological features are excessive lipid accumulation in hepatocytes and the subsequent lipotoxic damage. This not only drives the progression of the disease to hepatitis, liver fibrosis, and cirrhosis but also is significantly associated with an increased risk of hepatocellular carcinoma. NAFLD has become an increasingly serious global public health issue, and there is an urgent need to explore safe and effective prevention and treatment strategies. This study aimed to evaluate the intervention effect of kaempferol, a natural flavonoid compound, on palmitic acid (PA)-induced hepatocyte lipotoxicity.
Methods
A series of biochemical experiments were conducted to evaluate the effect of kaempferol on liver lipotoxicity.
Results
Our results demonstrated that kaempferol not only counteracted PA-induced suppression of hepatocyte proliferation and viability but also mitigated PA-triggered inflammatory response (TNF-α, IL-6, IL-1β) and oxidative stress (ROS). Importantly, we identified that these protective effects were achieved through the inhibition of ferroptosis, a novel form of cell death induced by PA. Mechanistically, kaempferol exerted its benefits primarily by activating the AMPK signaling pathway. AMPK activation led to a dual protective effect: first, by down-regulating the fatty acid transporter CD36 to reduce lipid accumulation; second, and more significantly, by effectively suppressing the ferroptosis cascade, thereby breaking the vicious cycle of lipid overload, oxidative stress, and cell death.
Conclusions
This new finding provides a novel perspective for understanding the efficacy of Kaempferol. This study not only confirms that kaempferol synergistically combats lipid metabolism disorders and ferroptosis through the "AMPK-CD36" axis but also provides a solid experimental basis and innovative theoretical support for the development of kaempferol as a drug for the prevention and treatment of fatty liver disease.
{"title":"Kaempferol alleviates high-fat-induced hepatocyte injury by inhibiting ferroptosis","authors":"Linjie Lou , Ren Ye , Yisheng Huang","doi":"10.1016/j.tice.2026.103323","DOIUrl":"10.1016/j.tice.2026.103323","url":null,"abstract":"<div><h3>Background</h3><div>Metabolic dysfunction-associated steatotic liver disease (MASLD) is a key manifestation of metabolic syndrome in the liver. Its core pathological features are excessive lipid accumulation in hepatocytes and the subsequent lipotoxic damage. This not only drives the progression of the disease to hepatitis, liver fibrosis, and cirrhosis but also is significantly associated with an increased risk of hepatocellular carcinoma. NAFLD has become an increasingly serious global public health issue, and there is an urgent need to explore safe and effective prevention and treatment strategies. This study aimed to evaluate the intervention effect of kaempferol, a natural flavonoid compound, on palmitic acid (PA)-induced hepatocyte lipotoxicity.</div></div><div><h3>Methods</h3><div>A series of biochemical experiments were conducted to evaluate the effect of kaempferol on liver lipotoxicity.</div></div><div><h3>Results</h3><div>Our results demonstrated that kaempferol not only counteracted PA-induced suppression of hepatocyte proliferation and viability but also mitigated PA-triggered inflammatory response (TNF-α, IL-6, IL-1β) and oxidative stress (ROS). Importantly, we identified that these protective effects were achieved through the inhibition of ferroptosis, a novel form of cell death induced by PA. Mechanistically, kaempferol exerted its benefits primarily by activating the AMPK signaling pathway. AMPK activation led to a dual protective effect: first, by down-regulating the fatty acid transporter CD36 to reduce lipid accumulation; second, and more significantly, by effectively suppressing the ferroptosis cascade, thereby breaking the vicious cycle of lipid overload, oxidative stress, and cell death.</div></div><div><h3>Conclusions</h3><div>This new finding provides a novel perspective for understanding the efficacy of Kaempferol. This study not only confirms that kaempferol synergistically combats lipid metabolism disorders and ferroptosis through the \"AMPK-CD36\" axis but also provides a solid experimental basis and innovative theoretical support for the development of kaempferol as a drug for the prevention and treatment of fatty liver disease.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"99 ","pages":"Article 103323"},"PeriodicalIF":2.5,"publicationDate":"2026-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145975977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-08DOI: 10.1016/j.tice.2026.103320
Fatima S. Alaryani
This study investigated the protective effects of banana flower extract (BFE) against aflatoxin B1 (AFB1)-induced oxidative stress, inflammation, and immune dysfunction in growing rabbits. One hundred and twenty rabbits were divided into four experimental groups: a control group (receiving a vehicle only), an AFB1 group (receiving 0.3 mg AFB1/kg diet), a BFE group (receiving 500 mg/kg banana flower extract), and an AFB1 and BFE group for eight weeks. The results showed that exposure to AFB1 resulted in reduced growth performance, along with elevated liver enzymes, blood lipids, and renal dysfunction (P < 0.05). Additionally, 8-OHdG levels were significantly higher in the AFB1 group, but BFE treatment significantly reduced this elevation (P < 0.05). AFB1 also caused a significant increase in oxidative stress (as indicated by higher MDA and PC levels) and a decrease in antioxidant enzyme activity (SOD, GPx, and TAC) and immune response (IgG and IgM). Pro-inflammatory responses were significantly increased by AFB1 exposure, while BFE treatment effectively prevented apoptosis (P < 0.05) and inflammation (P < 0.01) in the rabbits, and significantly improving immunoglobulin synthesis (P < 0.05). BFE protected against renal and intestinal structural damage induced by AFB1. Molecular docking studies revealed that gallic and protocatechuic acids interacted with BAX (binding energies: −4.17 and −6.78 kcal/mol, respectively), Caspase-3 (-4.28 and −7.38 kcal/mol, respectively), and SOD (-4.16 and −6.38 kcal/mol, respectively). These findings suggest that the compounds may play a role in modulating apoptosis and antioxidant defense. This study underscores the potential of utilizing by-product extracts, such as banana flower extract, to mitigate the adverse effects of aflatoxins in animals through their apoptotic and antioxidant properties.
{"title":"Mitigation conferred by banana flower extract against aflatoxin-induced oxidative stress, inflammation, apoptosis, molecular docking, and histological disturbances in rabbits","authors":"Fatima S. Alaryani","doi":"10.1016/j.tice.2026.103320","DOIUrl":"10.1016/j.tice.2026.103320","url":null,"abstract":"<div><div>This study investigated the protective effects of banana flower extract (BFE) against aflatoxin B1 (AFB1)-induced oxidative stress, inflammation, and immune dysfunction in growing rabbits. One hundred and twenty rabbits were divided into four experimental groups: a control group (receiving a vehicle only), an AFB1 group (receiving 0.3 mg AFB1/kg diet), a BFE group (receiving 500 mg/kg banana flower extract), and an AFB1 and BFE group for eight weeks. The results showed that exposure to AFB1 resulted in reduced growth performance, along with elevated liver enzymes, blood lipids, and renal dysfunction (P < 0.05). Additionally, 8-OHdG levels were significantly higher in the AFB1 group, but BFE treatment significantly reduced this elevation (P < 0.05). AFB1 also caused a significant increase in oxidative stress (as indicated by higher MDA and PC levels) and a decrease in antioxidant enzyme activity (SOD, GPx, and TAC) and immune response (IgG and IgM). Pro-inflammatory responses were significantly increased by AFB1 exposure, while BFE treatment effectively prevented apoptosis (P < 0.05) and inflammation (P < 0.01) in the rabbits, and significantly improving immunoglobulin synthesis (P < 0.05). BFE protected against renal and intestinal structural damage induced by AFB1. Molecular docking studies revealed that gallic and protocatechuic acids interacted with BAX (binding energies: −4.17 and −6.78 kcal/mol, respectively), Caspase-3 (-4.28 and −7.38 kcal/mol, respectively), and SOD (-4.16 and −6.38 kcal/mol, respectively). These findings suggest that the compounds may play a role in modulating apoptosis and antioxidant defense. This study underscores the potential of utilizing by-product extracts, such as banana flower extract, to mitigate the adverse effects of aflatoxins in animals through their apoptotic and antioxidant properties.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"99 ","pages":"Article 103320"},"PeriodicalIF":2.5,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145938894","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-08DOI: 10.1016/j.tice.2026.103315
Zeinab K. Aboghanima , Ashraf El Sharaby , Asmaa Aboelnour , Mohamed M.A. Abumandour , Ahmed G. Nomir
This study was carried out to explore the anatomical and microscopic features of the liver in shoveler ducks using gross and vascular anatomical casting, morphometric analysis, and histochemical techniques. This study was applied to twenty-six adult ducks. The liver, located in the middle-third of the coelomic cavity, had a larger right lobe and no further subdivided lobes, housing the gallbladder in a cystic fossa on the right lobe's visceral surface. The liver’s venous drainage occurs through the hepatic veins (right, left, and middle) along with accessory and umbilical veins. The intrahepatic portal system consisted of two portal veins: left and right. Hepatic arterial supply originated from the celiac artery, which divided into right and left branches for intrahepatic distribution. The right branch gave dorsal and ventral right hepatic arteries and continued as the right gastric artery, while the left branch formed the left gastric artery and gave left hepatic arteries. Histologically, the liver was surrounded by a thick connective tissue (CT) capsule with poorly defined lobules and polygonal hepatocytes around central veins. Hepatocytes expanded toward the subscapular region with few fat globules within the cytoplasm, displaying a larger nucleus, and the sinusoids were filled with erythrocytes. Histochemical analysis revealed a strong positive reaction to the PAS stain. Densely packed collagen fibers were demonstrated by Masson's trichrome stain in the capsule, around large blood vessels, and bile ducts.
{"title":"Anatomical and microscopic evaluation of the liver in migratory shoveler ducks (Spatula clypeata): A multi-modal study using gross anatomy, vascular casting, morphometric analysis, and histochemistry techniques","authors":"Zeinab K. Aboghanima , Ashraf El Sharaby , Asmaa Aboelnour , Mohamed M.A. Abumandour , Ahmed G. Nomir","doi":"10.1016/j.tice.2026.103315","DOIUrl":"10.1016/j.tice.2026.103315","url":null,"abstract":"<div><div>This study was carried out to explore the anatomical and microscopic features of the liver in shoveler ducks using gross and vascular anatomical casting, morphometric analysis, and histochemical techniques. This study was applied to twenty-six adult ducks. The liver, located in the middle-third of the coelomic cavity, had a larger right lobe and no further subdivided lobes, housing the gallbladder in a cystic fossa on the right lobe's visceral surface. The liver’s venous drainage occurs through the hepatic veins (right, left, and middle) along with accessory and umbilical veins. The intrahepatic portal system consisted of two portal veins: left and right. Hepatic arterial supply originated from the celiac artery, which divided into right and left branches for intrahepatic distribution. The right branch gave dorsal and ventral right hepatic arteries and continued as the right gastric artery, while the left branch formed the left gastric artery and gave left hepatic arteries. Histologically, the liver was surrounded by a thick connective tissue (CT) capsule with poorly defined lobules and polygonal hepatocytes around central veins. Hepatocytes expanded toward the subscapular region with few fat globules within the cytoplasm, displaying a larger nucleus, and the sinusoids were filled with erythrocytes. Histochemical analysis revealed a strong positive reaction to the PAS stain. Densely packed collagen fibers were demonstrated by Masson's trichrome stain in the capsule, around large blood vessels, and bile ducts.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"99 ","pages":"Article 103315"},"PeriodicalIF":2.5,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145975974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-08DOI: 10.1016/j.tice.2026.103318
Haiyan Yang , Lei Zhang , Haixia Qian
Cardiovascular diseases (CVDs) are the leading cause of death worldwide, far exceeding other diseases such as cancer. Myocardial injury is a key link in various CVDs; reducing myocardial injury is an effective means of preventing and treating CVDs. Mitochondrial dysfunction is the pathological basis of various CVDs. Mitophagy, as a process that selectively eliminates damaged or dysfunctional mitochondria, is of enormous significance in maintaining the normal function and structure of mitochondria in cardiomyocytes and alleviating myocardial injury. Therefore, this review systematically analyzes the role of mitophagy in myocardial injury, explores targeted intervention strategies, and hopes to provide a theoretical basis and effective therapeutic targets for clinical practice.
{"title":"The dual regulation of mitophagy in myocardial injury: From molecular mechanisms to targeted therapies","authors":"Haiyan Yang , Lei Zhang , Haixia Qian","doi":"10.1016/j.tice.2026.103318","DOIUrl":"10.1016/j.tice.2026.103318","url":null,"abstract":"<div><div>Cardiovascular diseases (CVDs) are the leading cause of death worldwide, far exceeding other diseases such as cancer. Myocardial injury is a key link in various CVDs; reducing myocardial injury is an effective means of preventing and treating CVDs. Mitochondrial dysfunction is the pathological basis of various CVDs. Mitophagy, as a process that selectively eliminates damaged or dysfunctional mitochondria, is of enormous significance in maintaining the normal function and structure of mitochondria in cardiomyocytes and alleviating myocardial injury. Therefore, this review systematically analyzes the role of mitophagy in myocardial injury, explores targeted intervention strategies, and hopes to provide a theoretical basis and effective therapeutic targets for clinical practice.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"99 ","pages":"Article 103318"},"PeriodicalIF":2.5,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145975979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-08DOI: 10.1016/j.tice.2026.103319
Fatma A. Madkour , Elsayed S.I. Mohammed , Eman E. El-Nahass , Mona M. Elwan , Ashraf S. Mohammad , Fatma Abdelhakeem
The tiger shark (Galeocerdo cuvier), a large apex predator fish, inhabits marine waters. It is also known for its dietary diversity and ecological importance as it plays a crucial role in maintaining the balance of the marine ecosystem. Despite the importance of this fish, no previous studies have reported the microscopic anatomy of its digestive system. The morphohistological features of the juvenile tiger shark stomach were thoroughly analyzed via histological, immunohistochemical, and ultrastructural procedures, as well as phylogenetic analysis. Histological results exhibited that the gastric mucosa was thrown into short, thick primary folds lined by columnar epithelium. Three types of cells lining the gastric glands: mucous neck cells, parietal cells, and chief cells. Histochemical staining revealed differential mucin distribution, as demonstrated by periodic acid-Schiff (PAS) and Alcian blue techniques (AB). Bromophenol blue (BPB) staining indicated high protein content in the keratin layer and mucosal epithelium. Immunohistochemical analysis displayed strong positive immunoreactivity in the surface epithelial cells and keratin layer, while the muscular layer showed no immunoreactivity. In semithin sections, telocytes (TCs) were identified across all gastric layers, recognized by their unique morphology and common distribution within the tunica muscularis. Scanning electron microscopy (SEM) demonstrated multiple well-developed longitudinal folds and concavities, and numerous openings were detected within the gastric mucosa. The study demonstrated the effectiveness of integrating multi-gene datasets and advanced phylogenetic methods in clarifying the complex evolutionary relationships of sharks. In conclusion, this study provides novel insights into juvenile tiger shark stomach morphology, highlighting the keratinized mucosal surface and the widespread presence of TCs, which underscore the potential protective and regulatory functions within the gastric wall.
{"title":"Insights into the stomach of tiger shark, Galeocerdo cuvier (Péron & Lesueur, 1822): Histochemical, ultrastructural, and phylogenetic analysis","authors":"Fatma A. Madkour , Elsayed S.I. Mohammed , Eman E. El-Nahass , Mona M. Elwan , Ashraf S. Mohammad , Fatma Abdelhakeem","doi":"10.1016/j.tice.2026.103319","DOIUrl":"10.1016/j.tice.2026.103319","url":null,"abstract":"<div><div>The tiger shark <em>(Galeocerdo cuvier)</em>, a large apex predator fish, inhabits marine waters. It is also known for its dietary diversity and ecological importance as it plays a crucial role in maintaining the balance of the marine ecosystem. Despite the importance of this fish, no previous studies have reported the microscopic anatomy of its digestive system. The morphohistological features of the juvenile tiger shark stomach were thoroughly analyzed via histological, immunohistochemical, and ultrastructural procedures, as well as phylogenetic analysis. Histological results exhibited that the gastric mucosa was thrown into short, thick primary folds lined by columnar epithelium. Three types of cells lining the gastric glands: mucous neck cells, parietal cells, and chief cells. Histochemical staining revealed differential mucin distribution, as demonstrated by periodic acid-Schiff (PAS) and Alcian blue techniques (AB). Bromophenol blue (BPB) staining indicated high protein content in the keratin layer and mucosal epithelium. Immunohistochemical analysis displayed strong positive immunoreactivity in the surface epithelial cells and keratin layer, while the muscular layer showed no immunoreactivity. In semithin sections, telocytes (TCs) were identified across all gastric layers, recognized by their unique morphology and common distribution within the tunica muscularis. Scanning electron microscopy (SEM) demonstrated multiple well-developed longitudinal folds and concavities, and numerous openings were detected within the gastric mucosa. The study demonstrated the effectiveness of integrating multi-gene datasets and advanced phylogenetic methods in clarifying the complex evolutionary relationships of sharks. In conclusion, this study provides novel insights into juvenile tiger shark stomach morphology, highlighting the keratinized mucosal surface and the widespread presence of TCs, which underscore the potential protective and regulatory functions within the gastric wall.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"99 ","pages":"Article 103319"},"PeriodicalIF":2.5,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145938892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-08DOI: 10.1016/j.tice.2026.103314
Amira Adly Kassab , Hani Ayman Alajou , Hadi Ali Alshihmani , Layan Suliman Hussein , Dareen Mahmoud Nofal , Zain Said Al-moudi , Leen Yousef Alkhateeb , Haneen Mustafa Alnasaa , Asmaa Mohamed Kharsa , Lara Mazen Aljabaly , Ruba Ahmad Alslehat , Adel Mohamed Aboregela , Darwish Badran
Oral mucositis is a common yet often overlooked complication of chemotherapy. Although paclitaxel (PTX) is a potent anticancer agent, it induces various pathologies in the oral tissues. Pumpkin seed oil (PSO) was prized significant pharmacological properties that can produce health-protective effects. The study aimed to highlight the effects of PTX on the dorsal tongue mucosa of rats and assess the alleviative role of PSO focusing on the underlying mechanisms. Forty rats were divided into: Control, PSO, PTX, and PTX + PSO. PTX was administered intraperitoneally at a dose of 2 mg/kg once weekly, while PSO was given orally at 1.5 ml/kg daily, both for 6 consecutive weeks. Tongue tissues were subjected to histological, immunohistochemical, biochemical and RT-qPCR analyses. PTX group exhibited a loss of the normal papillary architecture of the dorsal tongue mucosa. There was a statistically significant reduction in the epithelial thickness, the height and width of the papillae and proliferating cell nuclear antigen (PCNA) immunoreactivity. Malondialdehyde (MDA) levels were significantly elevated, while glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) levels were markedly decreased. A significant upregulation of NF-κβ, TNF-α, IL-1β, IL-18, and IL-6 mRNA expression was observed denoting markedly fired inflammatory cascade. PSO + PTX group showed significant mitigation of these molecular alterations which were translated into structural conservation with no significant difference when compared to the control group. PTX triggers inflammation and oxidative stress, leading to epithelial proliferation arrest. PSO, antioxidant and anti-inflammatory rescuer, effectively preserves the structural integrity of the dorsal tongue mucosa.
{"title":"Efficacy of pumpkin seed oil on paclitaxel-induced tongue mucosal injury in rat: Structural and biochemical insights","authors":"Amira Adly Kassab , Hani Ayman Alajou , Hadi Ali Alshihmani , Layan Suliman Hussein , Dareen Mahmoud Nofal , Zain Said Al-moudi , Leen Yousef Alkhateeb , Haneen Mustafa Alnasaa , Asmaa Mohamed Kharsa , Lara Mazen Aljabaly , Ruba Ahmad Alslehat , Adel Mohamed Aboregela , Darwish Badran","doi":"10.1016/j.tice.2026.103314","DOIUrl":"10.1016/j.tice.2026.103314","url":null,"abstract":"<div><div>Oral mucositis is a common yet often overlooked complication of chemotherapy. Although paclitaxel (PTX) is a potent anticancer agent, it induces various pathologies in the oral tissues. Pumpkin seed oil (PSO) was prized significant pharmacological properties that can produce health-protective effects. The study aimed to highlight the effects of PTX on the dorsal tongue mucosa of rats and assess the alleviative role of PSO focusing on the underlying mechanisms. Forty rats were divided into: Control, PSO, PTX, and PTX + PSO. PTX was administered intraperitoneally at a dose of 2 mg/kg once weekly, while PSO was given orally at 1.5 ml/kg daily, both for 6 consecutive weeks. Tongue tissues were subjected to histological, immunohistochemical, biochemical and RT-qPCR analyses. PTX group exhibited a loss of the normal papillary architecture of the dorsal tongue mucosa. There was a statistically significant reduction in the epithelial thickness, the height and width of the papillae and proliferating cell nuclear antigen (PCNA) immunoreactivity. Malondialdehyde (MDA) levels were significantly elevated, while glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) levels were markedly decreased. A significant upregulation of NF-κβ, TNF-α, IL-1β, IL-18, and IL-6 mRNA expression was observed denoting markedly fired inflammatory cascade. PSO + PTX group showed significant mitigation of these molecular alterations which were translated into structural conservation with no significant difference when compared to the control group. PTX triggers inflammation and oxidative stress, leading to epithelial proliferation arrest. PSO, antioxidant and anti-inflammatory rescuer, effectively preserves the structural integrity of the dorsal tongue mucosa.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"99 ","pages":"Article 103314"},"PeriodicalIF":2.5,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145938895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}