Reversibility and heritability of liver fibrosis:Implications for research and therapy

作     者：Hussein M Atta 

作者机构：Department of SurgeryFaculty of MedicineMinia UniversityEl-Minia 61519Egypt 

出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)

年 卷 期：2015年第21卷第17期

页      面：5138-5148页

核心收录：

学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

基　　金：Egyptian Science and Technology Development Fund under Project 1550 

主　　题：Epigenetics Epimutations Inheritance Livercirrhosis Hepatic stellate cells Histone modification DNA methylation MicroRNA Long noncoding RNA Transcription regulation 

摘      要：Liver fibrosis continues to be a major health problem worldwide due to lack of effective *** the etiology cannot be eliminated,liver fibrosis progresses to cirrhosis and eventually to liver failure or malignancy;both are associated with a fatal *** transplantation,the only curative therapy,is still mostly *** fibrosis was shown to be a reversible process;however,complete reversibility remains ***,the molecular markers of liver fibrosis were shown to be transmitted across *** mechanisms including DNA methylation,histone posttranslational modifications and noncoding RNA have emerged as major determinants of gene expression during liver fibrogenesis and ***,epigenetic mechanisms have been shown to be transmitted through mitosis and meiosis to daughter cells and subsequent ***,the exact epigenetic regulation of complete liver fibrosis resolution and inheritance has not been fully *** communication will highlight the recent advances in the search for delineating the mechanisms governing resolution of liver fibrosis and the potential for multigenerational and transgenerational transmission of fibrosis *** fact that epigenetic changes,unlike genetic mutations,are reversible and can be modulated pharmacologically underscores the unique opportunity to develop effective therapy to completely reverse liver fibrosis,to prevent the development of malignancy and to regulate heritability of fibrosis phenotype.