Pub Date : 2024-07-06DOI: 10.1016/j.gendis.2024.101373
{"title":"Prevalence of synonymous mutations in m6A modification sites in human cancers","authors":"","doi":"10.1016/j.gendis.2024.101373","DOIUrl":"10.1016/j.gendis.2024.101373","url":null,"abstract":"","PeriodicalId":12689,"journal":{"name":"Genes & Diseases","volume":"12 1","pages":"Article 101373"},"PeriodicalIF":6.9,"publicationDate":"2024-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141588491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Metabolic dysfunction-associated fatty liver disease (MAFLD) encompasses a spectrum of liver diseases ranging from metabolic dysfunction-associated fatty liver to metabolic dysfunction-associated steatohepatitis, which may progress to liver cirrhosis and hepatocellular carcinoma. Several mechanisms, including obesity, insulin resistance, dyslipidemia, inflammation, apoptosis, mitochondrial dysfunction, and reactive oxygen species, have been proposed to underlie the progression of MAFLD. Transcription factors are proteins that specifically bind to DNA sequences to regulate the transcription of target genes. Numerous transcription factors regulate MAFLD by modulating the transcription of genes involved in steatosis, inflammation, apoptosis, and fibrosis. Here, we review the pathological factors associated with MAFLD, with a particular emphasis on the transcription factors that contribute to the progression of MAFLD and their therapeutic implications.
代谢功能障碍相关性脂肪肝（MAFLD）包括一系列肝脏疾病，从代谢功能障碍相关性脂肪肝到代谢功能障碍相关性脂肪性肝炎，进而可能发展为肝硬化和肝细胞癌。肥胖、胰岛素抵抗、血脂异常、炎症、细胞凋亡、线粒体功能障碍和活性氧等几种机制被认为是 MAFLD 进展的基础。转录因子是与 DNA 序列特异性结合的蛋白质，可调节目标基因的转录。许多转录因子通过调节涉及脂肪变性、炎症、细胞凋亡和纤维化的基因转录来调控 MAFLD。在此，我们回顾了与 MAFLD 相关的病理因素，特别强调了导致 MAFLD 进展的转录因子及其治疗意义。
{"title":"Transcription factors, metabolic dysfunction-associated fatty liver disease, and therapeutic implications","authors":"Shuwei Hu, Yingjie Ai, Chencheng Hu, Fathima N. Cassim Bawa, Yanyong Xu","doi":"10.1016/j.gendis.2024.101372","DOIUrl":"https://doi.org/10.1016/j.gendis.2024.101372","url":null,"abstract":"Metabolic dysfunction-associated fatty liver disease (MAFLD) encompasses a spectrum of liver diseases ranging from metabolic dysfunction-associated fatty liver to metabolic dysfunction-associated steatohepatitis, which may progress to liver cirrhosis and hepatocellular carcinoma. Several mechanisms, including obesity, insulin resistance, dyslipidemia, inflammation, apoptosis, mitochondrial dysfunction, and reactive oxygen species, have been proposed to underlie the progression of MAFLD. Transcription factors are proteins that specifically bind to DNA sequences to regulate the transcription of target genes. Numerous transcription factors regulate MAFLD by modulating the transcription of genes involved in steatosis, inflammation, apoptosis, and fibrosis. Here, we review the pathological factors associated with MAFLD, with a particular emphasis on the transcription factors that contribute to the progression of MAFLD and their therapeutic implications.","PeriodicalId":12689,"journal":{"name":"Genes & Diseases","volume":"10 1","pages":""},"PeriodicalIF":6.8,"publicationDate":"2024-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141588493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-02DOI: 10.1016/j.gendis.2024.101370
Jiarui Bu, Zeyu Miao, Qing Yang
In recent years, the incidence and mortality rates of pancreatic cancer have been steadily increasing, and conventional therapies have shown a high degree of tolerance. Therefore, the search for new therapeutic targets remains a key issue in current research. Mitochondrial glutamic-oxaloacetic transaminase 2 (GOT2) is an important component of the malate-aspartate shuttle system, which plays an important role in the maintenance of cellular redox balance and amino acid metabolism, and has the potential to become a promising target for anti-cancer therapy. In this paper, we will elaborate on the metabolic and immune effects of GOT2 in pancreatic cancer based on existing studies, with a view to opening up new avenues for the treatment of pancreatic cancer.
{"title":"GOT2: New therapeutic target in pancreatic cancer","authors":"Jiarui Bu, Zeyu Miao, Qing Yang","doi":"10.1016/j.gendis.2024.101370","DOIUrl":"https://doi.org/10.1016/j.gendis.2024.101370","url":null,"abstract":"In recent years, the incidence and mortality rates of pancreatic cancer have been steadily increasing, and conventional therapies have shown a high degree of tolerance. Therefore, the search for new therapeutic targets remains a key issue in current research. Mitochondrial glutamic-oxaloacetic transaminase 2 (GOT2) is an important component of the malate-aspartate shuttle system, which plays an important role in the maintenance of cellular redox balance and amino acid metabolism, and has the potential to become a promising target for anti-cancer therapy. In this paper, we will elaborate on the metabolic and immune effects of GOT2 in pancreatic cancer based on existing studies, with a view to opening up new avenues for the treatment of pancreatic cancer.","PeriodicalId":12689,"journal":{"name":"Genes & Diseases","volume":"10 1","pages":""},"PeriodicalIF":6.8,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141585126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-06-28DOI: 10.1016/j.gendis.2024.101369
Xu Wang, Bei Yun, Zihan Zhang, Xiaoxi Wang, Yifan Wu, Yubo Hu, Shiyi Fang, Junjie Lv, Lina Chen, Wan Li
{"title":"DARG: An integrated knowledge base for analyzing addictive drug related genes","authors":"Xu Wang, Bei Yun, Zihan Zhang, Xiaoxi Wang, Yifan Wu, Yubo Hu, Shiyi Fang, Junjie Lv, Lina Chen, Wan Li","doi":"10.1016/j.gendis.2024.101369","DOIUrl":"https://doi.org/10.1016/j.gendis.2024.101369","url":null,"abstract":"","PeriodicalId":12689,"journal":{"name":"Genes & Diseases","volume":"107 1","pages":""},"PeriodicalIF":6.8,"publicationDate":"2024-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141588494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-06-22DOI: 10.1016/j.gendis.2024.101355
Xiaoya Zhang, Guiqiu Xie, Lang Rao, Chaoguang Tian
Protein citrullination involves the deimination of arginine or methylarginine residues in peptide chains to form citrulline by peptidyl arginine deiminases. This process is an important protein post-translational modification that affects molecular structure and function of various proteins, including histones. In recent years, protein citrullination has attracted widespread attention for its influence on gene transcription. Studies on the impact of protein citrullination modification on chromatin structure remodeling and the establishment of gene regulatory networks have made rapid progress. In this review, we briefly summarize the physiological functions of protein citrullination modification. Specifically, we comprehensively outline the latest progress in the study of the role of protein citrullination modification in gene transcription regulation, focusing on the interaction of protein citrullination with other post-translational modifications.
{"title":"Protein citrullination in gene transcription regulation and physiological implications","authors":"Xiaoya Zhang, Guiqiu Xie, Lang Rao, Chaoguang Tian","doi":"10.1016/j.gendis.2024.101355","DOIUrl":"https://doi.org/10.1016/j.gendis.2024.101355","url":null,"abstract":"Protein citrullination involves the deimination of arginine or methylarginine residues in peptide chains to form citrulline by peptidyl arginine deiminases. This process is an important protein post-translational modification that affects molecular structure and function of various proteins, including histones. In recent years, protein citrullination has attracted widespread attention for its influence on gene transcription. Studies on the impact of protein citrullination modification on chromatin structure remodeling and the establishment of gene regulatory networks have made rapid progress. In this review, we briefly summarize the physiological functions of protein citrullination modification. Specifically, we comprehensively outline the latest progress in the study of the role of protein citrullination modification in gene transcription regulation, focusing on the interaction of protein citrullination with other post-translational modifications.","PeriodicalId":12689,"journal":{"name":"Genes & Diseases","volume":"24 1","pages":""},"PeriodicalIF":6.8,"publicationDate":"2024-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141547897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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