Tissue & cell最新文献_第5页

3D mechanical stimulation modulates endothelial exosomes to promote fibroblast activation 三维机械刺激调节内皮外泌体促进成纤维细胞活化

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-01-12 DOI: 10.1016/j.tice.2026.103316

Ye Qiu , Zhenkun Lv , Xingying Zhu , Xiaoqian Yang , Jiaming Wan

Background

Mechanical forces play a crucial role in regulating cellular communication during tissue repair; however, it remains unclear how mechanical stimulation modulates endothelial exosome secretion and its effects on fibroblast activation.

Methods

In this study, endothelial cells were incorporated into 3D bioprinted tissue-engineered dermal constructs and cultured under static or mechanically stretched conditions. Exosomes were isolated from these cells, characterised, and applied to human dermal fibroblasts to assess their influence on proliferation, migration, and extracellular matrix formation. Data-independent acquisition proteomics was performed to analyse exosomal protein cargo and associated signalling pathways.

Results

Mechanical loading increased exosome secretion by approximately 2.5-fold without altering vesicle morphology. Functionally, mechanically stimulated exosomes enhanced fibroblast migration and type I collagen synthesis more significantly than controls. Proteomics profiling identified 4476 proteins in the exosomes, of which 677 were differentially expressed. Enrichment analysis revealed activation of the VEGF, HIF-1, Relaxin, and AGE–RAGE pathways, implicating roles in angiogenesis, metabolic regulation, and extracellular matrix remodelling.

Conclusion

These findings demonstrate that 3D mechanical stimulation not only augments the quantity of endothelial exosomes but also reshapes their molecular cargo, thereby enhancing biomechanical communication between endothelial cells and fibroblasts. Building on prior evidence that fibroblast-derived exosomes promote endothelial angiogenesis, we propose a bidirectional ‘mechanical stimulation–exosome–communication–tissue reconstruction’ loop, providing a theoretical foundation for optimising exosome-based strategies in skin tissue engineering.

在组织修复过程中，机械力在调节细胞通讯中起着至关重要的作用；然而，机械刺激如何调节内皮外泌体分泌及其对成纤维细胞激活的影响尚不清楚。方法将内皮细胞植入生物3D打印的组织工程真皮结构中，并在静态或机械拉伸条件下进行培养。从这些细胞中分离出外泌体，对其进行表征，并应用于人类真皮成纤维细胞，以评估其对增殖、迁移和细胞外基质形成的影响。数据独立获取蛋白质组学进行分析外泌体蛋白货物和相关的信号通路。结果在不改变囊泡形态的情况下，机械负荷使外泌体分泌增加约2.5倍。在功能上，机械刺激的外泌体比对照组更显著地增强了成纤维细胞的迁移和I型胶原的合成。蛋白质组学分析在外泌体中鉴定出4476种蛋白质，其中677种是差异表达的。富集分析显示VEGF、HIF-1、Relaxin和AGE-RAGE通路的激活，暗示其在血管生成、代谢调节和细胞外基质重塑中的作用。结论三维机械刺激不仅增加了内皮外泌体的数量，而且重塑了它们的分子货物，从而增强了内皮细胞和成纤维细胞之间的生物力学通讯。基于成纤维细胞衍生的外泌体促进内皮血管生成的先前证据，我们提出了一个双向的“机械刺激-外泌体-通讯-组织重建”回路，为优化皮肤组织工程中基于外泌体的策略提供了理论基础。

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引用次数: 0

Ovulation-derived extracellular vesicles exhibit sustained oncogenic influence on the exposed fallopian tube fimbrial cells after drainage into peritoneal cavity 排卵来源的细胞外囊泡在引流到腹腔后对暴露的输卵管毛细胞表现出持续的致癌影响

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-01-11 DOI: 10.1016/j.tice.2026.103327

Aye Aye Khine , Pao-Chu Chen , Ying-Hsi Chen , Hsuan-Shun Huang , Tang-Yuan Chu

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.

排卵损伤输卵管上皮细胞（FTE），促进细胞转化，促进高级别浆液性卵巢癌（HGSC）的发展。虽然排卵卵泡液来源的细胞外囊泡（EVs）已被证明具有细胞转化活性，但尚不清楚这些EVs是否在排卵后持续存在于腹腔，可能延长其暴露时间并增强其对输卵管上皮（FTE）细胞的转化作用。在这项研究中，我们收集了排卵前后女性的卵泡液（FF）和腹膜液（PF），并使用非锚定菌落生长试验研究了排卵来源的ev对FTE细胞的致癌潜力。我们发现，相较于排卵前的PF，排卵后的PF表现出更高的细胞转化活性，这种活性的增强与排卵后PF中EVs浓度和蛋白质含量的增加有关。从同一患者的不同排卵卵泡中获得的FF样品显示出一致的转化活性，并且FF或排卵后PF衍生的EVs在不同转化阶段的FTE细胞中保持这种转化能力。我们的研究揭示了一种新的机制，通过释放到腹膜微环境中的ev的持续致癌作用，排卵可能有助于FTE的转化。这一发现为未来癌症的预防、治疗和潜在的诊断性生物标志物研究提供了新的视角和方向。

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引用次数: 0

Tumor endothelial cells revisited: Their crucial role in tumor progression 肿瘤内皮细胞：它们在肿瘤进展中的关键作用。

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-01-09 DOI: 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.

肿瘤周围的血管不仅是营养物质、氧气和代谢物的运输通道，也是肿瘤转移的途径。本文综述了肿瘤内皮细胞的组织和细胞来源，分析了其特点，总结了其在肿瘤进展和转移中的作用。由于其独特的特性，肿瘤内皮细胞成为旨在阻止肿瘤血管形成的抗血管生成治疗的靶点。新兴的治疗策略旨在调节肿瘤内皮细胞和免疫细胞，不仅可以阻断血管生成，还可以增强肿瘤内效应细胞的募集和激活。

引用次数: 0

The role of neprilysin in musculoskeletal diseases 神经球蛋白在肌肉骨骼疾病中的作用。

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-01-09 DOI: 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.

Neprilysin （NEP）是一种膜结合的内肽酶，可降解多种底物，包括利钠肽、缓动肽和p物质。NEP分布于心脏、肾脏和大脑等多个器官，调节多种生理过程。本文阐明了NEP在成骨、软骨和肌分化过程中的作用，以及它在分化过程中的时间特异性表达。我们关注NEP如何调节骨骼肌疾病的关键途径，探索潜在的机制，并证明临床症状改善。NEP降解促炎神经肽，从而减轻局部炎症。此外，NEP已被证明是负责内源性阿片类药物的降解，从而有助于调节疼痛。在骨骼肌损伤修复中，NEP促进动物间充质干细胞的成骨、成软骨和成肌分化，实现组织再生。通过讨论临床批准的NEP抑制剂和激活剂对骨骼肌疾病的治疗效果，发现NEP抑制剂Shakubitril在软骨发育不良动物模型中促进软骨生长板增厚和骨骼生长。NEP激活剂比NEP抑制剂更能促进阉割大鼠的肌肉生长。这篇综述强调了NEP在骨骼肌生长发育中的作用，不同骨骼肌疾病中NEP水平的变化及其对疾病进展的影响。最后对NEP相关药物在骨骼肌疾病中的疗效进行了探讨，希望为骨骼肌疾病的治疗提供新的途径。

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引用次数: 0

Research on rhubarb's natural components and their potential for treating chronic kidney disease 大黄天然成分及其治疗慢性肾脏疾病潜力的研究

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-01-09 DOI: 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.

肾纤维化是慢性肾脏疾病的主要病理改变，其特点是细胞外基质过度沉积、肾小管细胞上皮-间质转化、成纤维细胞增殖和活化等。已经证明，大黄，一种可能的天然物质，可以用作慢性肾脏疾病的常规或补充治疗。通过多种药理作用，包括天然成分的抗炎和抗氧化特性，它可能针对肾纤维化并产生其作用。本文简要介绍了肾纤维化的病理过程，系统总结了近年来利用大黄天然成分治疗肾纤维化的研究进展，为研制抗肾纤维化药物提供了新的思路。

引用次数: 0

Kaempferol alleviates high-fat-induced hepatocyte injury by inhibiting ferroptosis 山奈酚通过抑制铁下垂减轻高脂诱导的肝细胞损伤

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-01-09 DOI: 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.

背景：代谢功能障碍相关脂肪变性肝病（MASLD）是肝脏代谢综合征的重要表现。其核心病理特征是肝细胞内脂质过度积聚和随后的脂毒性损伤。这不仅会导致疾病进展为肝炎、肝纤维化和肝硬化，而且还与肝细胞癌的风险增加显著相关。NAFLD已成为日益严重的全球性公共卫生问题，迫切需要探索安全有效的预防和治疗策略。本研究旨在评价天然类黄酮化合物山奈酚对棕榈酸（PA）诱导的肝细胞脂毒性的干预作用。方法通过一系列生化实验评价山奈酚对肝脏脂肪毒性的影响。结果山奈酚不仅可以抵消pa诱导的肝细胞增殖和活力的抑制，还可以减轻pa引发的炎症反应（TNF-α、IL-6、IL-1β）和氧化应激（ROS）。重要的是，我们发现这些保护作用是通过抑制铁下垂来实现的，铁下垂是PA诱导的一种新型细胞死亡形式。从机制上讲，山奈酚主要通过激活AMPK信号通路发挥其益处。AMPK激活产生双重保护作用：一是下调脂肪酸转运蛋白CD36，减少脂质积累；其次，更重要的是，通过有效抑制铁下垂级联，从而打破脂质超载、氧化应激和细胞死亡的恶性循环。结论这一新发现为了解山奈酚的疗效提供了新的视角。本研究不仅证实了山奈酚通过“AMPK-CD36”轴协同对抗脂质代谢紊乱和铁下沉，也为山奈酚作为预防和治疗脂肪肝的药物的开发提供了坚实的实验基础和创新的理论支持。

{"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}

引用次数: 0

Mitigation conferred by banana flower extract against aflatoxin-induced oxidative stress, inflammation, apoptosis, molecular docking, and histological disturbances in rabbits 香蕉花提取物对家兔黄曲霉毒素诱导的氧化应激、炎症、细胞凋亡、分子对接和组织学紊乱的缓解作用

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-01-08 DOI: 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.

本研究探讨了香蕉花提取物（BFE）对黄曲霉毒素B1 （AFB1）诱导的氧化应激、炎症和免疫功能障碍的保护作用。将120只家兔分为4个实验组：对照组（只给药）、AFB1组（给0.3 mg AFB1/kg日粮）、BFE组（给500 mg/kg香蕉花提取物）、AFB1和BFE组，持续8周。结果表明，暴露于AFB1导致生长性能下降，同时肝酶、血脂升高和肾功能障碍（P <； 0.05）。此外，AFB1组8-OHdG水平显著升高，但BFE治疗显著降低了这一升高（P <； 0.05）。AFB1还引起氧化应激显著增加（MDA和PC水平升高），抗氧化酶活性（SOD、GPx和TAC）和免疫反应（IgG和IgM）降低。AFB1暴露显著增加了兔的促炎反应，而BFE处理有效地阻止了兔的细胞凋亡（P <； 0.05）和炎症（P <； 0.01），并显著提高了免疫球蛋白的合成（P <； 0.05）。BFE对AFB1引起的肾脏和肠道结构损伤具有保护作用。分子对接研究表明，没食子酸和原儿茶酸与BAX（结合能分别为−4.17和−6.78 kcal/mol）、Caspase-3（结合能分别为-4.28和−7.38 kcal/mol）和SOD（结合能分别为-4.16和−6.38 kcal/mol）相互作用。这些发现提示这些化合物可能在调节细胞凋亡和抗氧化防御中起作用。这项研究强调了利用副产物提取物的潜力，如香蕉花提取物，通过其细胞凋亡和抗氧化特性来减轻黄曲霉毒素对动物的不良影响。

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引用次数: 0

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 迁徙铲鸭（Spatula clypeata）肝脏的解剖和显微评价：一项多模式研究，使用大体解剖、血管铸型、形态计量学分析和组织化学技术

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-01-08 DOI: 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.

本研究采用大体和血管解剖铸型、形态计量学分析和组织化学技术，探讨了铲鸭肝脏的解剖和显微特征。本研究以26只成年野鸭为试验对象。肝脏位于体腔的中间三分之一，有一个较大的右叶，没有进一步细分的叶，在右叶内脏表面的囊窝中容纳胆囊。肝静脉引流通过肝静脉（右、左、中）以及副静脉和脐静脉。肝内门静脉系统由左、右两条门静脉组成。肝动脉供应起源于腹腔动脉，分为左、右支分布于肝内。右支形成右肝背动脉和腹侧动脉，继续形成胃右动脉；左支形成胃左动脉，形成肝左动脉。组织学上，肝脏被厚的结缔组织（CT）包膜包围，小叶界限不清，中央静脉周围有多角形肝细胞。肝细胞向肩胛下区扩张，胞质内脂肪球较少，细胞核较大，窦状区充盈红细胞。组织化学分析显示PAS染色强烈阳性反应。马松三色染色显示被膜、大血管和胆管周围胶原纤维密集堆积。

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引用次数: 0

The dual regulation of mitophagy in myocardial injury: From molecular mechanisms to targeted therapies 心肌损伤中线粒体自噬的双重调控：从分子机制到靶向治疗

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-01-08 DOI: 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.

心血管疾病（cvd）是全世界导致死亡的主要原因，远远超过癌症等其他疾病。心肌损伤是各种心血管疾病的关键环节；减少心肌损伤是预防和治疗心血管疾病的有效手段。线粒体功能障碍是各种心血管疾病的病理基础。线粒体自噬作为一种选择性清除受损或功能失调线粒体的过程，对维持心肌细胞线粒体的正常功能和结构，减轻心肌损伤具有重要意义。因此，本文系统分析线粒体自噬在心肌损伤中的作用，探索有针对性的干预策略，希望能为临床实践提供理论依据和有效的治疗靶点。

引用次数: 0

Insights into the stomach of tiger shark, Galeocerdo cuvier (Péron & Lesueur, 1822): Histochemical, ultrastructural, and phylogenetic analysis 虎鲨胃的洞察，Galeocerdo cuvier (p<s:1> & Lesueur, 1822)：组织化学、超微结构和系统发育分析

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-01-08 DOI: 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.

虎鲨（Galeocerdo cuvier）是一种大型的顶端捕食鱼，栖息在海水中。它也因其饮食多样性和生态重要性而闻名，因为它在维持海洋生态系统的平衡方面起着至关重要的作用。尽管这种鱼很重要，但之前没有研究报道过其消化系统的微观解剖结构。通过组织病理学、免疫组织化学、超微结构和系统发育分析，对虎鲨幼胃的形态组织学特征进行了全面分析。组织学结果显示胃粘膜呈短而厚的原代褶皱，内衬柱状上皮。胃腺有三种细胞：黏液颈细胞、壁细胞和主细胞。组织化学染色显示不同的粘蛋白分布，如周期性酸希夫（PAS）和阿利新蓝技术（AB）所示。溴酚蓝（BPB）染色显示角蛋白层和粘膜上皮蛋白含量高。免疫组化分析显示，表面上皮细胞和角蛋白层有较强的阳性免疫反应性，而肌肉层无免疫反应性。在半薄切片中，在所有胃层中都发现了远端细胞（tc），通过其独特的形态和在肌层内的共同分布来识别。扫描电镜（SEM）显示胃粘膜内有多个发育良好的纵向褶皱和凹陷，并发现许多开口。该研究证明了整合多基因数据集和先进的系统发育方法在阐明鲨鱼复杂的进化关系方面的有效性。总之，本研究为幼年虎鲨胃形态提供了新的见解，突出了角化的粘膜表面和广泛存在的TCs，这强调了胃壁内潜在的保护和调节功能。

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引用次数: 0