Mitochondrial dysfunction in fibrotic diseases

• Published in: Cell death discovery Vol. 6; no. 1; p. 80
• Main Authors: Li, Xinyu, Zhang, Wei, Cao, Qingtai, Wang, Zeyu, Zhao, Mingyi, Xu, Linyong, Zhuang, Quan
• Format: Journal Article
• Language: English
• Published: United States Springer Nature B.V 05.09.2020; Nature Publishing Group UK
• Subjects: DNA damage; Fibrosis; Membrane potential; Mitochondrial DNA; Review; Structure-function relationships; Mitochondria; Metabolic disorders
• ISSN: 2058-7716; 2058-7716
• DOI: 10.1038/s41420-020-00316-9

Although fibrosis is a common pathological feature of most end-stage organ diseases, its pathogenesis remains unclear. There is growing evidence that mitochondrial dysfunction contributes to the development and progression of fibrosis. The heart, liver, kidney and lung are highly oxygen-consuming organs that are sensitive to mitochondrial dysfunction. Moreover, the fibrotic process of skin and islet is closely related to mitochondrial dysfunction as well. This review summarized emerging mechanisms related to mitochondrial dysfunction in different fibrotic organs and tissues above. First, it highlighted the important elucidation of mitochondria morphological changes, mitochondrial membrane potential and structural damage, mitochondrial DNA (mtDNA) damage and reactive oxidative species (ROS) production, etc. Second, it introduced the abnormality of mitophagy and mitochondrial transfer also contributed to the fibrotic process. Therefore, with gaining the increasing knowledge of mitochondrial structure, function, and origin, we could kindle a new era for the diagnostic and therapeutic strategies of many fibrotic diseases based on mitochondrial dysfunction.