纤维化
脂毒性
脂肪酸代谢
脂质代谢
生物
生物化学
脂肪酸
医学
生物信息学
癌症研究
病理
内分泌学
糖尿病
胰岛素抵抗
作者
Seonghwan Hwang,Ki Wung Chung
标识
DOI:10.1007/s12272-021-01352-4
摘要
Fibrosis is defined by abnormal accumulation of extracellular matrix, which can affect virtually every organ system under diseased conditions. Fibrotic tissue remodeling often leads to organ dysfunction and is highly associated with increased morbidity and mortality. The disease burden caused by fibrosis is substantial, and the medical need for effective antifibrotic therapies is essential. Significant progress has been made in understanding the molecular mechanism and pathobiology of fibrosis, such as transforming growth factor-β (TGF-β)-mediated signaling pathways. However, owing to the complex and dynamic properties of fibrotic disorders, there are currently no therapeutic options that can prevent or reverse fibrosis. Recent studies have revealed that alterations in fatty acid metabolic processes are common mechanisms and core pathways that play a central role in different fibrotic disorders. Excessive lipid accumulation or defective fatty acid oxidation is associated with increased lipotoxicity, which directly contributes to the development of fibrosis. Genetic alterations or pharmacologic targeting of fatty acid metabolic processes have great potential for the inhibition of fibrosis development. Furthermore, mechanistic studies have revealed active interactions between altered metabolic processes and fibrosis development. Several well-known fibrotic factors change the lipid metabolic processes, while altered metabolic processes actively participate in fibrosis development. This review summarizes the recent evidence linking fatty acid metabolism and fibrosis, and provides new insights into the pathogenesis of fibrotic diseases for the development of drugs for fibrosis prevention and treatment.
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