{"title":"Thyroid-Stimulating Hormone: An Important Target for the Prevention of Nonalcoholic Fatty Liver Disease.","authors":"Z Wang, H Wang, H Sun","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Non-alcoholic fatty liver disease (NAFLD) is one of the leading causes of cirrhosis and liver cancer. Its global prevalence increases annually, significantly affecting quality of life. Only a few patients manage to alleviate NAFLD through lifestyle modifications. The pathogenic mechanisms and therapeutic targets of this disease remain inadequately explored. In recent years, many studies highlighted a close relationship between the thyroid-stimulating hormone (TSH) and NAFLD. TSH has been shown to promote fat accumulation in the liver by participating in the ab initio synthesis, uptake and secretion of lipids. Moreover, TSH exacerbates hepatocyte inflammation and fibrosis by inducing endoplasmic reticulum stress and promoting the release of inflammatory factors. Although some of the conclusions remain controversial and are subject to debate, exploring the connection and possible pathways between TSH and NAFLD is crucial. Such research could advance early clinical prevention and intervention strategies, thereby reducing the incidence of severe NAFLD-associated comorbidities. Therefore, this review aims to summarize currently available evidence on the association between TSH and NAFLD focusing on the following objectives: elucidating the relationship between TSH and NAFLD; TSH may be a potential target for NAFLD prevention; exploring potential molecular targets that could block TSH-mediated promotion of NAFLD.</p>","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"74 2","pages":"175-187"},"PeriodicalIF":1.9000,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12148143/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Physiological research","FirstCategoryId":"3","ListUrlMain":"","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"PHYSIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Non-alcoholic fatty liver disease (NAFLD) is one of the leading causes of cirrhosis and liver cancer. Its global prevalence increases annually, significantly affecting quality of life. Only a few patients manage to alleviate NAFLD through lifestyle modifications. The pathogenic mechanisms and therapeutic targets of this disease remain inadequately explored. In recent years, many studies highlighted a close relationship between the thyroid-stimulating hormone (TSH) and NAFLD. TSH has been shown to promote fat accumulation in the liver by participating in the ab initio synthesis, uptake and secretion of lipids. Moreover, TSH exacerbates hepatocyte inflammation and fibrosis by inducing endoplasmic reticulum stress and promoting the release of inflammatory factors. Although some of the conclusions remain controversial and are subject to debate, exploring the connection and possible pathways between TSH and NAFLD is crucial. Such research could advance early clinical prevention and intervention strategies, thereby reducing the incidence of severe NAFLD-associated comorbidities. Therefore, this review aims to summarize currently available evidence on the association between TSH and NAFLD focusing on the following objectives: elucidating the relationship between TSH and NAFLD; TSH may be a potential target for NAFLD prevention; exploring potential molecular targets that could block TSH-mediated promotion of NAFLD.
期刊介绍:
Physiological Research is a peer reviewed Open Access journal that publishes articles on normal and pathological physiology, biochemistry, biophysics, and pharmacology.
Authors can submit original, previously unpublished research articles, review articles, rapid or short communications.
Instructions for Authors - Respect the instructions carefully when submitting your manuscript. Submitted manuscripts or revised manuscripts that do not follow these Instructions will not be included into the peer-review process.
The articles are available in full versions as pdf files beginning with volume 40, 1991.
The journal publishes the online Ahead of Print /Pre-Press version of the articles that are searchable in Medline and can be cited.