生物
细胞生物学
氧化应激
粒线体疾病
生物信息学
线粒体DNA
氧化磷酸化
线粒体生物发生
线粒体融合
粒体自噬
作者
Ying Tan,Fengfan Xia,Lulan Li,Xiaojie Peng,Wenqian Liu,Yaoyuan Zhang,Haihong Fang,Zhenhua Zeng,Zhongqing Chen
摘要
Mitochondria maintain mitochondrial homeostasis through continuous fusion and fission, that is, mitochondrial dynamics, which is precisely mediated by mitochondrial fission and fusion proteins, including dynamin-related protein 1 (Drp1), mitofusin 1 and 2 (Mfn1/2), and optic atrophy 1 (OPA1). When the mitochondrial fission and fusion of cardiomyocytes are out of balance, they will cause their own morphology and function disorders, which damage the structure and function of the heart, are involved in the occurrence and progression of cardiovascular disease such as ischemia-reperfusion injury (IRI), septic cardiomyopathy, and diabetic cardiomyopathy. In this paper, we focus on the latest findings regarding the molecular features and regulatory mechanisms of mitochondrial dynamic disorder in cardiovascular pathologies. Finally, we will address how these findings can be applied to improve the treatment of cardiovascular disease.
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