Clinical and Molecular Hepatology最新文献

{"title":"Current status and perspective on molecular targets and therapeutic intervention strategy in hepatic ischemia-reperfusion injury.","authors":"Jia Liu, Ranyi Luo, Yinhao Zhang, Xiaojiaoyang Li","doi":"10.3350/cmh.2024.0222","DOIUrl":"10.3350/cmh.2024.0222","url":null,"abstract":"<p><p>Hepatic ischemia‒reperfusion injury (HIRI) is a common and inevitable complication of hepatic trauma, liver resection, or liver transplantation. It contributes to postoperative organ failure or tissue rejection, eventually affecting patient prognosis and overall survival. The pathological mechanism of HIRI is highly complex and has not yet been fully elucidated. The proposed underlying mechanisms include mitochondrial damage, oxidative stress imbalance, abnormal cell death, immune cell hyperactivation, intracellular inflammatory disorders and other complex events. In addition to serious clinical limitations, available antagonistic drugs and specific treatment regimens are still lacking. Therefore, there is an urgent need to not only clarify the exact etiology of HIRI but also reveal the possible reactions and bottlenecks of existing drugs, helping to reduce morbidity and shorten hospitalizations. We analyzed the possible underlying mechanism of HIRI, discussed various outcomes among different animal models and explored neglected potential therapeutic strategies for HIRI treatment. By thoroughly reviewing and analyzing the literature on HIRI, we gained a comprehensive understanding of the current research status in related fields and identified valuable references for future clinical and scientific investigations.</p>","PeriodicalId":10275,"journal":{"name":"Clinical and Molecular Hepatology","volume":null,"pages":null},"PeriodicalIF":14.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11540405/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141466588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correspondence to editorial on \"Macrophage ATG16L1 expression suppresses metabolic dysfunction-associated steatohepatitis progression by promoting lipophagy\".","authors":"Qi Wang, Qingfa Bu, Haoming Zhou, Ling Lu","doi":"10.3350/cmh.2024.0470","DOIUrl":"10.3350/cmh.2024.0470","url":null,"abstract":"","PeriodicalId":10275,"journal":{"name":"Clinical and Molecular Hepatology","volume":null,"pages":null},"PeriodicalIF":14.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11540352/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141554246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correspondence to editorial on \"Hepatocellular carcinoma prediction model performance decreases with long-term antiviral therapy in chronic hepatitis B patients\".","authors":"Xiaoqian Xu, Hong You, Jidong Jia, Yuanyuan Kong","doi":"10.3350/cmh.2024.0552","DOIUrl":"10.3350/cmh.2024.0552","url":null,"abstract":"","PeriodicalId":10275,"journal":{"name":"Clinical and Molecular Hepatology","volume":null,"pages":null},"PeriodicalIF":14.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11540353/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141747512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metformin and statins and their role in reducing hepatocellular carcinoma risk: Randomized trials are needed: Editorial on \"Metformin and statins reduce hepatocellular carcinoma risk in chronic hepatitis C patients with failed antiviral therapy\".","authors":"Paul Y Kwo","doi":"10.3350/cmh.2024.0425","DOIUrl":"10.3350/cmh.2024.0425","url":null,"abstract":"","PeriodicalId":10275,"journal":{"name":"Clinical and Molecular Hepatology","volume":null,"pages":null},"PeriodicalIF":14.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11540391/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141300170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Macrophage ATG16L1: Potential candidate for metabolic dysfunction-associated steatohepatitis treatment: Editorial on \"Macrophage ATG16L1 expression suppresses metabolic dysfunction-associated steatohepatitis progression by promoting lipophagy\".","authors":"Junjie Yu","doi":"10.3350/cmh.2024.0443","DOIUrl":"10.3350/cmh.2024.0443","url":null,"abstract":"","PeriodicalId":10275,"journal":{"name":"Clinical and Molecular Hepatology","volume":null,"pages":null},"PeriodicalIF":14.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11540392/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141418156","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correspondence to editorial on \"Dynamic analysis of acute deterioration in chronic liver disease patients using modified quick sequential organ failure assessment\".","authors":"Do Seon Song, Dong Joon Kim","doi":"10.3350/cmh.2024.0448","DOIUrl":"10.3350/cmh.2024.0448","url":null,"abstract":"","PeriodicalId":10275,"journal":{"name":"Clinical and Molecular Hepatology","volume":null,"pages":null},"PeriodicalIF":14.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11540344/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141418155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"UBE2S promotes glycolysis in hepatocellular carcinoma by enhancing E3 enzyme-independent polyubiquitination of VHL.","authors":"Renyu Zhang, Can Li, Shuai Zhang, Lingmin Kong, Zekun Liu, Yixiao Guo, Ying Sun, Cong Zhang, Yule Yong, Jianjun Lv, Meng Lu, Man Liu, Dong Wu, Tianjiao Zhang, Haijiao Yang, Ding Wei, Zhinan Chen, Huijie Bian","doi":"10.3350/cmh.2024.0236","DOIUrl":"10.3350/cmh.2024.0236","url":null,"abstract":"<p><strong>Background/aims: </strong>Ubiquitination is widely involved in the progression of hepatocellular carcinoma (HCC) by regulating various cellular processes. However, systematic strategies for screening core ubiquitin-related genes, clarifying their functions and mechanisms, and ultimately developing potential therapeutics for patients with HCC are still lacking.</p><p><strong>Methods: </strong>Cox and LASSO regression analyses were performed to construct a ubiquitin-related gene prediction model for HCC. Loss- and gain-of-function studies, transcriptomic and metabolomics analysis were used to explore the function and mechanism of UBE2S on HCC cell glycolysis and growth.</p><p><strong>Results: </strong>Based on 1,423 ubiquitin-related genes, a four-gene signature was successfully constructed to evaluate the prognosis of patients with HCC. UBE2S was identified in this signature with the potential to predict the survival of patients with HCC. E2F2 transcriptionally upregulated UBE2S expression by directly binding to its promoter. UBE2S positively regulated glycolysis in a HIF-1α-dependent manner, thus promoting the proliferation of HCC cells. Mechanistically, UBE2S enhanced K11-linkage polyubiquitination at lysine residues 171 and 196 of VHL independent of E3 ligase, thereby indirectly stabilizing HIF-1α protein levels by mediating the degradation of VHL by the proteasome. In particular, the combination of cephalomannine, a small molecule compound that inhibits the expression of UBE2S, and PX-478, an inhibitor of HIF-1α, significantly improved the anti-tumor efficacy.</p><p><strong>Conclusion: </strong>UBE2S is identified as a key biomarker in HCC among the thousands of ubiquitin-related genes and promotes glycolysis by E3 enzyme-independent ubiquitination, thus serving as a therapeutic target for the treatment of HCC.</p>","PeriodicalId":10275,"journal":{"name":"Clinical and Molecular Hepatology","volume":null,"pages":null},"PeriodicalIF":14.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11540382/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141445735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reply to correspondence on \"Protein-centric omics analysis reveals circulating complements linked to non-viral liver diseases as potential therapeutic targets\".","authors":"Mohammad Saeid Rezaee-Zavareh, Naomy Kim, Ju Dong Yang","doi":"10.3350/cmh.2024.0320","DOIUrl":"10.3350/cmh.2024.0320","url":null,"abstract":"","PeriodicalId":10275,"journal":{"name":"Clinical and Molecular Hepatology","volume":null,"pages":null},"PeriodicalIF":14.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11540390/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140848417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynamic change of metabolic dysfunction-associated steatotic liver disease in chronic hepatitis C patients after viral eradication: A nationwide registry study in Taiwan.","authors":"Chung-Feng Huang, Chia-Yen Dai, Yi-Hung Lin, Chih-Wen Wang, Tyng-Yuan Jang, Po-Cheng Liang, Tzu-Chun Lin, Pei-Chien Tsai, Yu-Ju Wei, Ming-Lun Yeh, Ming-Yen Hsieh, Chao-Kuan Huang, Jee-Fu Huang, Wan-Long Chuang, Ming-Lung Yu","doi":"10.3350/cmh.2024.0414","DOIUrl":"10.3350/cmh.2024.0414","url":null,"abstract":"<p><strong>Background/aims: </strong>Steatotic liver disease (SLD) is a common manifestation in chronic hepatitis C (CHC). Metabolic alterations in CHC are associated with metabolic dysfunction-associated steatotic liver disease (MASLD). We aimed to elucidate whether hepatitis C virus (HCV) eradication mitigates MASLD occurrence or resolution.</p><p><strong>Methods: </strong>We enrolled 5,840 CHC patients whose HCV was eradicated by direct-acting antivirals in a nationwide HCV registry. MASLD and the associated cardiometabolic risk factors (CMRFs) were evaluated at baseline and 6 months after HCV cure.</p><p><strong>Results: </strong>There were 2,147 (36.8%) patients with SLD, and 1,986 (34.0%) of them met the MASLD criteria before treatment. After treatment, HbA1c (6.0% vs. 5.9%, P<0.001) and BMI (24.8 kg/m2 vs. 24.7 kg/m2, P<0.001) decreased, whereas HDL-C (49.1 mg/dL vs. 51.9 mg/dL, P<0.001) and triglycerides (102.8 mg/dL vs. 111.9 mg/dL, P<0.001) increased significantly. The proportion of patients with SLD was 37.5% after HCV eradication, which did not change significantly compared with the pretreatment status. The percentage of the patients who had post-treatment MASLD was 34.8%, which did not differ significantly from the pretreatment status (P=0.17). Body mass index (BMI) (odds ratio [OR] 0.89; 95% confidence intervals [CI] 0.85-0.92; P<0.001) was the only factor associated with MASLD resolution. In contrast, unfavorable CMRFs, including BMI (OR 1.10; 95% CI 1.06-1.14; P<0.001) and HbA1c (OR 1.19; 95% CI 1.04-1.35; P=0.01), were independently associated with MASLD development after HCV cure.</p><p><strong>Conclusion: </strong>HCV eradication mitigates MASLD in CHC patients. CMRF surveillance is mandatory for CHC patients with metabolic alterations, which are altered after HCV eradication and predict the evolution of MASLD.</p>","PeriodicalId":10275,"journal":{"name":"Clinical and Molecular Hepatology","volume":null,"pages":null},"PeriodicalIF":14.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11540343/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141787422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-term gastrointestinal and hepatobiliary outcomes of COVID-19: A multinational population-based cohort study from South Korea, Japan, and the UK.","authors":"Kwanjoo Lee, Jaeyu Park, Jinseok Lee, Myeongcheol Lee, Hyeon Jin Kim, Yejun Son, Sang Youl Rhee, Lee Smith, Masoud Rahmati, Jiseung Kang, Hayeon Lee, Yeonjung Ha, Dong Keon Yon","doi":"10.3350/cmh.2024.0203","DOIUrl":"10.3350/cmh.2024.0203","url":null,"abstract":"<p><strong>Background/aims: </strong>Considering emerging evidence on long COVID, comprehensive analyses of the post-acute complications of SARS-CoV-2 infection in the gastrointestinal and hepatobiliary systems are needed. We aimed to investigate the impact of COVID-19 on the long-term risk of gastrointestinal and hepatobiliary diseases and other digestive abnormalities.</p><p><strong>Methods: </strong>We used three large-scale population-based cohorts: the Korean cohort (discovery cohort), the Japanese cohort (validation cohort-A), and the UK Biobank (validation cohort-B). A total of 10,027,506 Korean, 12,218,680 Japanese, and 468,617 UK patients aged ≥20 years who had SARS-CoV-2 infection between 2020 and 2021 were matched to non-infected controls. Seventeen gastrointestinal and eight hepatobiliary outcomes as well as nine other digestive abnormalities following SARS-CoV-2 infection were identified and compared with controls.</p><p><strong>Results: </strong>The discovery cohort revealed heightened risks of gastrointestinal diseases (HR 1.15; 95% CI 1.08-1.22), hepatobiliary diseases (HR 1.30; 95% CI 1.09-1.55), and other digestive abnormalities (HR 1.05; 95% CI 1.01-1.10) beyond the first 30 days of infection, after exposure-driven propensity score-matching. The risk was pronounced according to the COVID-19 severity. The SARS-CoV-2 vaccination was found to lower the risk of gastrointestinal diseases but did not affect hepatobiliary diseases and other digestive disorders. The results derived from validation cohorts were consistent. The risk profile was most pronounced during the initial 3 months; however, it persisted for >6 months in validation cohorts, but not in the discovery cohort.</p><p><strong>Conclusion: </strong>The incidence of gastrointestinal disease, hepatobiliary disease, and other digestive abnormalities increased in patients with SARS-CoV-2 infection during the post-acute phase.</p>","PeriodicalId":10275,"journal":{"name":"Clinical and Molecular Hepatology","volume":null,"pages":null},"PeriodicalIF":14.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11540398/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}