RNA methylations in hepatic fibrosis, a gradually emerging new treatment strategy
Abstract Background Hepatic fibrosis (HF) is a pathological process caused by excessive accumulation of extracellular matrix caused by a series of causes, leading to the formation of fiber scar. RNA methylation is a newly discovered epigenetic modification that exists widely in eukaryotes and prokar...
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BMC
2023-07-01
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Series: | Cell & Bioscience |
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Online Access: | https://doi.org/10.1186/s13578-023-01066-8 |
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author | Chenglong Cheng Yajie Wu Xin Wang Qiuyun Xue Yurong Huang Faxue Liao Xiao Wang Qiangjun Duan Chenggui Miao |
author_facet | Chenglong Cheng Yajie Wu Xin Wang Qiuyun Xue Yurong Huang Faxue Liao Xiao Wang Qiangjun Duan Chenggui Miao |
author_sort | Chenglong Cheng |
collection | DOAJ |
description | Abstract Background Hepatic fibrosis (HF) is a pathological process caused by excessive accumulation of extracellular matrix caused by a series of causes, leading to the formation of fiber scar. RNA methylation is a newly discovered epigenetic modification that exists widely in eukaryotes and prokaryotes and plays a crucial role in the pathogenesis of many diseases. Results The occurrence and development of HF are regulated by many factors, including excessive deposition of extracellular matrix, activation of hepatic stellate cells, inflammation, and oxidative stress. RNA methylations of different species have become a crucial regulatory mode of transcript expression, And participate in the pathogenesis of tumors, nervous system diseases, autoimmune diseases, and other diseases. In addition, there are five common types of RNA methylation, but only m6A plays a crucial regulatory role in HF. The pathophysiological regulation of m6A on HF is achieved by the combination of the methylated transferase, demethylated enzyme, and methylated reading protein. Conclusions RNA methylated methyltransferase, demethylase, and reading protein extensively affect the pathological mechanism of HF, which may be a new therapeutic and diagnostic target, representing a new class of therapeutic strategies. |
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id | doaj.art-b5d2f69209b344ffbb7b29cdd82d9cfb |
institution | Directory Open Access Journal |
issn | 2045-3701 |
language | English |
last_indexed | 2024-03-13T00:39:58Z |
publishDate | 2023-07-01 |
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series | Cell & Bioscience |
spelling | doaj.art-b5d2f69209b344ffbb7b29cdd82d9cfb2023-07-09T11:26:14ZengBMCCell & Bioscience2045-37012023-07-0113111410.1186/s13578-023-01066-8RNA methylations in hepatic fibrosis, a gradually emerging new treatment strategyChenglong Cheng0Yajie Wu1Xin Wang2Qiuyun Xue3Yurong Huang4Faxue Liao5Xiao Wang6Qiangjun Duan7Chenggui Miao8Department of Pharmacology, School of Integrated Chinese and Western Medicine, Anhui University of Chinese MedicineDepartment of Pharmacology, School of Integrated Chinese and Western Medicine, Anhui University of Chinese MedicineDepartment of Pharmacology, School of Integrated Chinese and Western Medicine, Anhui University of Chinese MedicineDepartment of Pharmacology, School of Integrated Chinese and Western Medicine, Anhui University of Chinese MedicineDepartment of Pharmacology, School of Integrated Chinese and Western Medicine, Anhui University of Chinese MedicineDepartment of Orthopaedics, The First Affiliated Hospital, Anhui Medical UniversityDepartment of Clinical Nursing, School of Nursing, Anhui University of Chinese MedicineDepartment of Experimental (Practical Training) Teaching Center, School of Integrated Chinese and Western Medicine, Anhui University of Chinese MedicineDepartment of Pharmacology, School of Integrated Chinese and Western Medicine, Anhui University of Chinese MedicineAbstract Background Hepatic fibrosis (HF) is a pathological process caused by excessive accumulation of extracellular matrix caused by a series of causes, leading to the formation of fiber scar. RNA methylation is a newly discovered epigenetic modification that exists widely in eukaryotes and prokaryotes and plays a crucial role in the pathogenesis of many diseases. Results The occurrence and development of HF are regulated by many factors, including excessive deposition of extracellular matrix, activation of hepatic stellate cells, inflammation, and oxidative stress. RNA methylations of different species have become a crucial regulatory mode of transcript expression, And participate in the pathogenesis of tumors, nervous system diseases, autoimmune diseases, and other diseases. In addition, there are five common types of RNA methylation, but only m6A plays a crucial regulatory role in HF. The pathophysiological regulation of m6A on HF is achieved by the combination of the methylated transferase, demethylated enzyme, and methylated reading protein. Conclusions RNA methylated methyltransferase, demethylase, and reading protein extensively affect the pathological mechanism of HF, which may be a new therapeutic and diagnostic target, representing a new class of therapeutic strategies.https://doi.org/10.1186/s13578-023-01066-8EpigeneticsHepatic fibrosisRNA methylationN6-methyladenosineHepatic stellate cells |
spellingShingle | Chenglong Cheng Yajie Wu Xin Wang Qiuyun Xue Yurong Huang Faxue Liao Xiao Wang Qiangjun Duan Chenggui Miao RNA methylations in hepatic fibrosis, a gradually emerging new treatment strategy Cell & Bioscience Epigenetics Hepatic fibrosis RNA methylation N6-methyladenosine Hepatic stellate cells |
title | RNA methylations in hepatic fibrosis, a gradually emerging new treatment strategy |
title_full | RNA methylations in hepatic fibrosis, a gradually emerging new treatment strategy |
title_fullStr | RNA methylations in hepatic fibrosis, a gradually emerging new treatment strategy |
title_full_unstemmed | RNA methylations in hepatic fibrosis, a gradually emerging new treatment strategy |
title_short | RNA methylations in hepatic fibrosis, a gradually emerging new treatment strategy |
title_sort | rna methylations in hepatic fibrosis a gradually emerging new treatment strategy |
topic | Epigenetics Hepatic fibrosis RNA methylation N6-methyladenosine Hepatic stellate cells |
url | https://doi.org/10.1186/s13578-023-01066-8 |
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