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作 者:Sisi Fan Wei Chen Linxi Chen Lanfang Li
出 处:《Acta Biochimica et Biophysica Sinica》2022年第4期590-592,共3页生物化学与生物物理学报(英文版)
基 金:the grants from the National Natural Science Foundation of China(No.81970431);the Hunan Provincial Natural Science Foundation of China(No.2020JJ4079)。
摘 要:Fibrosis,the self-repair process of the body after tissue damage,is a common pathological feature of many chronic inflammatory diseases.It occurs in a variety of organs,leading to structural destruction and hypofunction,and even organ failure.Fibrosis in organ tissues is characterized by chronic inflammation,excessive accumulation of extracellular matrix(ECM)components,and the decrease of parenchymal cells.Fibrosis is caused by persistent infections,toxins,autoimmune diseases,radiation,and mechanical injury.To date,there are various therapeutic strategies for organ fibrosis,such as changing lifestyle,using antiviral drugs,anti-inflammatory treatment,using interferon,and organ transplantation.Currently,there are only two FDA-approved drugs for the treatment of idiopathic pulmonary fibrosis(IPF),i.e.,pirfenidone and nintedanib.Nevertheless,the mechanisms of action of these drugs are not fully understood,the cost is high,and there is no way to prevent or reverse the disease process.Consequently,it is extremely important for us to better understand the pathogenesis of fibrosis,strengthen the screening and evaluation of new drugs,and improve the existing drugs.And it can also help us to treat and prevent fibrosis in the future.
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