{"title":"Advances in Ubiquitination and Proteostasis in Retinal Degeneration","authors":"Jia Wei, Xiaona Chen, Yingyue Xiong, Yali Gao","doi":"10.31083/j.fbl2907260","DOIUrl":"https://doi.org/10.31083/j.fbl2907260","url":null,"abstract":"","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"67 13","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141817890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
T. Kirichenko, A. Bogatyreva, Elena V. Gerasimova, Tatiana V. Popkova, Y. Markina, A. Markin, D. Gerasimova, A. N. Orekhov
{"title":"Inflammatory Response of Monocytes/Macrophages in Patients with Systemic Sclerosis","authors":"T. Kirichenko, A. Bogatyreva, Elena V. Gerasimova, Tatiana V. Popkova, Y. Markina, A. Markin, D. Gerasimova, A. N. Orekhov","doi":"10.31083/j.fbl2907259","DOIUrl":"https://doi.org/10.31083/j.fbl2907259","url":null,"abstract":"","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"25 19","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141814515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stella Aikaterini Kyriakoudi, Despoina Chatzi, I. Dermitzakis, Sofia Gargani, M. Manthou, S. Meditskou, Paschalis Theotokis
{"title":"Genetic Identity of Neural Crest Cell Differentiation in Tissue and Organ Development","authors":"Stella Aikaterini Kyriakoudi, Despoina Chatzi, I. Dermitzakis, Sofia Gargani, M. Manthou, S. Meditskou, Paschalis Theotokis","doi":"10.31083/j.fbl2907261","DOIUrl":"https://doi.org/10.31083/j.fbl2907261","url":null,"abstract":"","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"22 8","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141815954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
According to the research, obesity is associated with hyperlipidemia, hypertension, and type 2 diabetes mellitus, which are grouped as metabolic syndrome. Notably, under the obese status, the adipocyte could accumulate excessive lipid as lipid droplets (LDs), leading the dysfunctional fat mass. Recently, emerging evidence has shown that the cell death-inducing DNA fragmentation factor 45-like effector protein (CIDE) family played an important role in regulating lipid metabolism. In addition, diverse CIDE proteins were also confirmed to influence the intracellular lipid metabolism, such as within adipocyte, hepatocyte, and macrophage. Nevertheless, the results which showed the regulatory influence of CIDE proteins are significantly contradictory from in vitro experiments and in vivo clinical studies. Similarly, recent studies have changed the perception of these proteins, redefining them as regulators of lipid droplet dynamics and fat metabolism, which contribute to a healthy metabolic phenotype in humans. However, the underlying mechanisms by which the diverse CIDE proteins alter lipid metabolism are not elucidated. In the current review, the understandings of CIDE proteins in lipid catabolism were well-summarized. On the other hand, the relatively mechanisms were also proposed for the further understandings of the CIDE protein family.
{"title":"Relationship between the Cell Death-Inducing DNA Fragmentation Factor 45-Like Effector Protein Family and the Risk of Dyslipidemia","authors":"Jingjin Song, Huiyuan Kang, Ye Cheng","doi":"10.31083/j.fbl2907258","DOIUrl":"https://doi.org/10.31083/j.fbl2907258","url":null,"abstract":"According to the research, obesity is associated with hyperlipidemia, hypertension, and type 2 diabetes mellitus, which are grouped as metabolic syndrome. Notably, under the obese status, the adipocyte could accumulate excessive lipid as lipid droplets (LDs), leading the dysfunctional fat mass. Recently, emerging evidence has shown that the cell death-inducing DNA fragmentation factor 45-like effector protein (CIDE) family played an important role in regulating lipid metabolism. In addition, diverse CIDE proteins were also confirmed to influence the intracellular lipid metabolism, such as within adipocyte, hepatocyte, and macrophage. Nevertheless, the results which showed the regulatory influence of CIDE proteins are significantly contradictory from in vitro experiments and in vivo clinical studies. Similarly, recent studies have changed the perception of these proteins, redefining them as regulators of lipid droplet dynamics and fat metabolism, which contribute to a healthy metabolic phenotype in humans. However, the underlying mechanisms by which the diverse CIDE proteins alter lipid metabolism are not elucidated. In the current review, the understandings of CIDE proteins in lipid catabolism were well-summarized. On the other hand, the relatively mechanisms were also proposed for the further understandings of the CIDE protein family.","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":" 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141822951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Inflammatory bowel disease (IBD) is a chronic and recurrent inflammatory disease of the intestinal tract. The complex pathophysiological mechanisms of IBD include genetic susceptibility, environmental factors, and abnormal immune response of the gut microbiota. Gut microbiota forms a metabolic organ that contributes to human health by performing various physiological functions. The development of IBD is closely linked to the imbalance of gut microbiota. In IBD patients, this imbalance is mainly characterized by an increased abundance of pro-inflammatory microorganisms, specifically enteropathogenic bacteria. Pyroptosis is a form of programmed cell death that can be initiated by microbial infection or host factors. It occurs mostly after intracellular infection with bacteria or pathogens. Other than cell death, its primary effect is to release inflammatory mediators that trigger an inflammatory response in the host. Pyroptosis is an important component of innate immunity and can protect against intracellular risk factors via the inflammatory response. However, excessive activation can cause disease. Previous studies of IBD have indicated a complex relationship between gut microbiota and pyroptosis. Some enteropathogenic bacteria can activate the host’s immune system to clear infected cells. This inhibits the proliferation of enteropathogenic bacteria by inducing pyroptosis and restoring the balance of gut microbiota. However, the initial inflammatory response and damage to the integrity of the intestinal barrier are crucial factors that elicit the onset of IBD and favor its progression. This review summarizes research on the role of several common enteropathogenic bacteria in the development of IBD through their induction of host cell pyroptosis. A better understanding of the complex interactions between gut microbiota and pyroptosis should lead to the identification of new targets and treatment options for IBD.
{"title":"Novel Insights into the Interaction between Enteropathogenic Bacteria, Pyroptosis and IBD","authors":"Zhengyang Bao, Yimai Deng, Zhengtao Qian, Yaoyao Zhuang","doi":"10.31083/j.fbl2907254","DOIUrl":"https://doi.org/10.31083/j.fbl2907254","url":null,"abstract":"Inflammatory bowel disease (IBD) is a chronic and recurrent inflammatory disease of the intestinal tract. The complex pathophysiological mechanisms of IBD include genetic susceptibility, environmental factors, and abnormal immune response of the gut microbiota. Gut microbiota forms a metabolic organ that contributes to human health by performing various physiological functions. The development of IBD is closely linked to the imbalance of gut microbiota. In IBD patients, this imbalance is mainly characterized by an increased abundance of pro-inflammatory microorganisms, specifically enteropathogenic bacteria. Pyroptosis is a form of programmed cell death that can be initiated by microbial infection or host factors. It occurs mostly after intracellular infection with bacteria or pathogens. Other than cell death, its primary effect is to release inflammatory mediators that trigger an inflammatory response in the host. Pyroptosis is an important component of innate immunity and can protect against intracellular risk factors via the inflammatory response. However, excessive activation can cause disease. Previous studies of IBD have indicated a complex relationship between gut microbiota and pyroptosis. Some enteropathogenic bacteria can activate the host’s immune system to clear infected cells. This inhibits the proliferation of enteropathogenic bacteria by inducing pyroptosis and restoring the balance of gut microbiota. However, the initial inflammatory response and damage to the integrity of the intestinal barrier are crucial factors that elicit the onset of IBD and favor its progression. This review summarizes research on the role of several common enteropathogenic bacteria in the development of IBD through their induction of host cell pyroptosis. A better understanding of the complex interactions between gut microbiota and pyroptosis should lead to the identification of new targets and treatment options for IBD.","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":" 866","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141823493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yanbo Xiao, Xuan Zhu, Qun Li, Zongkang Wang, Qiaojuan Zuo, Xun Liu, Jin Tan
{"title":"m6A-Mediated IRS1 Regulates the Development of Oral Squamous Cell Carcinoma through p53/Line-1 Signaling","authors":"Yanbo Xiao, Xuan Zhu, Qun Li, Zongkang Wang, Qiaojuan Zuo, Xun Liu, Jin Tan","doi":"10.31083/j.fbl2907257","DOIUrl":"https://doi.org/10.31083/j.fbl2907257","url":null,"abstract":"","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":"121 19","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141822067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Methyl Syringate: A Primary Driving Factor in Manuka Honeys Ability to Ameliorate Neutrophil Intracellular ROS Activity and NETosis","authors":"Evan N. Main, James C. Huang, Gary L Bowlin","doi":"10.31083/j.fbl2907255","DOIUrl":"https://doi.org/10.31083/j.fbl2907255","url":null,"abstract":"","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":" 443","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141823801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Le Vu Duy, Pham Thi Huong, Nguyen Trung Nam, Do Thi Trang, Nghiem Thi Minh Chau, Tran Thi Phuong Thao, Nguyen Huy Hoang, Nguyen Thien Tao, Can Van Mao, Nguyen Thi Xuan
Background : Prostate cancer (PCa) is one of the most common malignant tumors of the male urinary system, and its incidence and mortality rates have been increasing worldwide. Benign prostatic hyperplasia (BPH) represents stromal and epithelial cell proliferation in the prostate in elderly males. Abnormal activation of inflammation-related signalling molecules, such as toll-like receptor 4 (TLR4) and Janus kinase/signal transducers and activators of transcription (JAK/STAT) has been linked to the initiation and progression of various human diseases including PCa and BPH. Cylindromatosis (CYLD) gene alterations are associated with PCa progression. In this study, the contribution of CYLD , JAK2 , and TLR4 gene variants to PCa and BPH risks and their associations with prostate-specific antigen (PSA) levels, immunophenotype, and clinical features in Vietnamese men were determined. Methods : A total of 102 patients with PCa, 65 with BPH, and 114 healthy controls were enrolled. The immunophenotype was analyzed by flow cytometry, cytokine secretion by enzyme-linked immunosorbent assay (ELISA), and gene variants by DNA sequencing. Results : Lower levels of transforming growth factor β (TGF-β ) and higher numbers of CD13 + CD117 − and CD56 + CD25 + cells were observed in the PCa group than in the BPH group. Genetic analysis of the CYLD gene identified five single nucleotide polymorphisms (SNPs), of which c.2351-47 C > T, c.2351-46A > T, and rs1971432171 T > G had significantly higher frequencies in PCa patients than in the control and BPH groups. Sequencing of the TLR4 gene revealed five nucleotide changes, in which the rs2149356 SNP showed an increased risk for both PCa and BPH and the c.331-206 SNP had a reduced risk for PCa. Importantly, the expansion of activated natural killer (NK) cells and higher levels of PSA were found in PCa patients carrying the CT genotype of the CYLD c.2351-47 compared to those with the wild-type genotype. Conclusion : Activation of NK cells in CYLD -sensitive PCa patients was associated with serum PSA release and the CYLD c.2351-47 variant may be a significant risk factor for prostatitis in PCa patients.
{"title":"Associations of CYLD, JAK2 and TLR4 Genotypes with PSA Levels and Immunophenotype in Benign Prostatic Hyperplasia and Prostate Cancer","authors":"Le Vu Duy, Pham Thi Huong, Nguyen Trung Nam, Do Thi Trang, Nghiem Thi Minh Chau, Tran Thi Phuong Thao, Nguyen Huy Hoang, Nguyen Thien Tao, Can Van Mao, Nguyen Thi Xuan","doi":"10.31083/j.fbl2907256","DOIUrl":"https://doi.org/10.31083/j.fbl2907256","url":null,"abstract":"Background : Prostate cancer (PCa) is one of the most common malignant tumors of the male urinary system, and its incidence and mortality rates have been increasing worldwide. Benign prostatic hyperplasia (BPH) represents stromal and epithelial cell proliferation in the prostate in elderly males. Abnormal activation of inflammation-related signalling molecules, such as toll-like receptor 4 (TLR4) and Janus kinase/signal transducers and activators of transcription (JAK/STAT) has been linked to the initiation and progression of various human diseases including PCa and BPH. Cylindromatosis (CYLD) gene alterations are associated with PCa progression. In this study, the contribution of CYLD , JAK2 , and TLR4 gene variants to PCa and BPH risks and their associations with prostate-specific antigen (PSA) levels, immunophenotype, and clinical features in Vietnamese men were determined. Methods : A total of 102 patients with PCa, 65 with BPH, and 114 healthy controls were enrolled. The immunophenotype was analyzed by flow cytometry, cytokine secretion by enzyme-linked immunosorbent assay (ELISA), and gene variants by DNA sequencing. Results : Lower levels of transforming growth factor β (TGF-β ) and higher numbers of CD13 + CD117 − and CD56 + CD25 + cells were observed in the PCa group than in the BPH group. Genetic analysis of the CYLD gene identified five single nucleotide polymorphisms (SNPs), of which c.2351-47 C > T, c.2351-46A > T, and rs1971432171 T > G had significantly higher frequencies in PCa patients than in the control and BPH groups. Sequencing of the TLR4 gene revealed five nucleotide changes, in which the rs2149356 SNP showed an increased risk for both PCa and BPH and the c.331-206 SNP had a reduced risk for PCa. Importantly, the expansion of activated natural killer (NK) cells and higher levels of PSA were found in PCa patients carrying the CT genotype of the CYLD c.2351-47 compared to those with the wild-type genotype. Conclusion : Activation of NK cells in CYLD -sensitive PCa patients was associated with serum PSA release and the CYLD c.2351-47 variant may be a significant risk factor for prostatitis in PCa patients.","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":" 919","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141823202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Saliva is a promising biological fluid for the diagnosis and monitoring of diseases, including breast cancer. To study the composition of saliva, a complex of “omics” technologies is used: genomics, transcriptomics, proteomics, metabolomics and microbiomics. In this review, we systematized all known “omics” in their application to saliva analysis in breast cancer in order to understand how complete the picture is provided by the combination of different areas of research and to identify missing links. It has been shown that studies of saliva in breast cancer are chaotic and unsystematic. Inconsistency of sample sizes and high heterogeneity of breast cancer were identified. The main tasks that need to be solved for the complete and harmonious development of salivaomics in a new direction—“salivaonkoomics” are formulated. Thus, it is necessary to systematize and unify the study of biomarkers within each area of “omics”, including sample size and its homogeneity, a list of methods and approaches, a list of biomarkers, reproducibility of results, and the ability to transfer results to other samples. It is important to expand the number of components of “omics” by adding new methods (for example, spectralomics, etc.), as well as studying the relationships between different “omics” technologies (interactomics). All this together will allow the study of saliva not only in breast cancer but also in many other pathologies to a qualitatively new level.
{"title":"Salivary Biomarkers in Breast Cancer: From Salivaomics to Salivaoncoomics","authors":"L. Bel’skaya, E. I. Dyachenko","doi":"10.31083/j.fbl2907253","DOIUrl":"https://doi.org/10.31083/j.fbl2907253","url":null,"abstract":"Saliva is a promising biological fluid for the diagnosis and monitoring of diseases, including breast cancer. To study the composition of saliva, a complex of “omics” technologies is used: genomics, transcriptomics, proteomics, metabolomics and microbiomics. In this review, we systematized all known “omics” in their application to saliva analysis in breast cancer in order to understand how complete the picture is provided by the combination of different areas of research and to identify missing links. It has been shown that studies of saliva in breast cancer are chaotic and unsystematic. Inconsistency of sample sizes and high heterogeneity of breast cancer were identified. The main tasks that need to be solved for the complete and harmonious development of salivaomics in a new direction—“salivaonkoomics” are formulated. Thus, it is necessary to systematize and unify the study of biomarkers within each area of “omics”, including sample size and its homogeneity, a list of methods and approaches, a list of biomarkers, reproducibility of results, and the ability to transfer results to other samples. It is important to expand the number of components of “omics” by adding new methods (for example, spectralomics, etc.), as well as studying the relationships between different “omics” technologies (interactomics). All this together will allow the study of saliva not only in breast cancer but also in many other pathologies to a qualitatively new level.","PeriodicalId":503756,"journal":{"name":"Frontiers in Bioscience-Landmark","volume":" 21","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141830076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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