Recent progress on obesity-induced myocardial remodeling and its possible mechanism of mitochondrial dyshomeostasis / 生理学报
Acta Physiologica Sinica
;
(6): 216-224, 2019.
Artigo
em Chinês
| WPRIM
| ID: wpr-777194
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.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Patologia
/
Espécies Reativas de Oxigênio
/
Dinâmica Mitocondrial
/
Mitocôndrias
/
Miocárdio
/
Obesidade
Tipo de estudo:
Fatores de risco
Limite:
Humanos
Idioma:
Chinês
Revista:
Acta Physiologica Sinica
Ano de publicação:
2019
Tipo de documento:
Artigo
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