粒体自噬
线粒体DNA
线粒体
氧化磷酸化
发病机制
线粒体内膜
生物
细胞生物学
机制(生物学)
疾病
生物信息学
医学
遗传学
基因
内科学
生物化学
免疫学
细胞凋亡
哲学
认识论
自噬
作者
Abdallah Iddy Chaurembo,Na Xing,Francis Chanda,Yuan Li,Huijuan Zhang,Li-dan Fu,Jian-yuan Huang,Yun-jing Xu,Wenhui Deng,Haodong Cui,Xin-yue Tong,Chi Shu,Han-bin Lin,Kai-xuan Lin
标识
DOI:10.1016/j.phrs.2024.107164
摘要
The impact of mitochondrial dysfunction on the pathogenesis of cardiovascular disease is increasing. However, the precise underlying mechanism remains unclear. Mitochondria produce cellular energy through oxidative phosphorylation while regulating calcium homeostasis, cellular respiration, and the production of biosynthetic chemicals. Nevertheless, problems related to cardiac energy metabolism, defective mitochondrial proteins, mitophagy, and structural changes in mitochondrial membranes can cause cardiovascular diseases via mitochondrial dysfunction. Mitofilin is a critical inner mitochondrial membrane protein that maintains cristae structure and facilitates protein transport while linking the inner mitochondrial membrane, outer mitochondrial membrane, and mitochondrial DNA transcription. Researchers believe that mitofilin may be a therapeutic target for treating cardiovascular diseases, particularly cardiac mitochondrial dysfunctions. In this review, we highlight current findings regarding the role of mitofilin in the pathogenesis of cardiovascular diseases and potential therapeutic compounds targeting mitofilin.
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