Recent progress on obesity-induced myocardial remodeling and its possible mechanism of mitochondrial dyshomeostasis.
- Author:
Qing WU
1
;
Run-Qing XUE
1
;
Man XU
1
;
Yi LU
1
;
Xiao-Jiang YU
1
;
Long-Zhu LIU
1
;
Wei-Jin ZANG
2
Author Information
1. Department of Pharmacology, Xi'an Jiaotong University Health Science Center, Xi'an 710061, China.
2. Department of Pharmacology, Xi'an Jiaotong University Health Science Center, Xi'an 710061, China. zwj@xjtu.edu.cn.
- Publication Type:Journal Article
- MeSH:
Humans;
Mitochondria;
pathology;
Mitochondrial Dynamics;
Myocardium;
pathology;
Obesity;
physiopathology;
Reactive Oxygen Species
- From:
Acta Physiologica Sinica
2019;71(2):216-224
- CountryChina
- Language:Chinese
-
Abstract:
Obesity is an important risk factor for cardiovascular diseases, which can lead to a variety of cardiovascular diseases including myocardial remodeling. Obesity may induce myocardial dysfunction by affecting hemodynamics, inducing autonomic imbalance, adipose tissue dysfunction, and mitochondrial dyshomeostasis. The key necessary biochemical functions for metabolic homeostasis are performed in mitochondria, and mitochondrial homeostasis is considered as one of the key determinants for cell viability. Mitochondrial homeostasis is regulated by dynamic regulation of mitochondrial fission and fusion, as well as mitochondrial cristae remodeling, biogenesis, autophagy, and oxidative stress. The mitochondrial fission-fusion and morphological changes of mitochondrial cristae maintain the integrity of the mitochondrial structure. The mitochondria maintain a "healthy" state by balancing biogenesis and autophagy, while reactive oxygen species can act as signaling molecules to regulate intracellular signaling. The excessive accumulation of lipids and lipid metabolism disorder in obesity leads to mitochondrial dyshomeostasis, which activate the apoptotic cascade and lead to myocardial remodeling. In this review, we provide an overview of the recent research progress on obesity-induced myocardial remodeling and its possible mechanism of mitochondrial dyshomeostasis.
