粒体自噬
品脱1
自噬
细胞生物学
线粒体
生物
帕金
DNAJA3公司
线粒体融合
机制(生物学)
线粒体DNA
粒线体疾病
遗传学
细胞凋亡
医学
疾病
帕金森病
基因
哲学
认识论
病理
作者
Haoran Wang,Wenjun Luo,Haoyu Chen,Zhiduan Cai,Guibin Xu
出处
期刊:Mitochondrion
[Elsevier BV]
日期:2024-01-19
卷期号:75: 101847-101847
被引量:11
标识
DOI:10.1016/j.mito.2024.101847
摘要
Mitochondrial dynamics and autophagy play essential roles in normal cellular physiological activities, while abnormal mitochondrial dynamics and mitochondrial autophagy can cause cancer and related disorders. Abnormal mitochondrial dynamics usually occur in parallel with mitochondrial autophagy. Both have been reported to have a synergistic effect and can therefore complement or inhibit each other. Progress has been made in understanding the classical mitochondrial PINK1/Parkin pathway and mitochondrial dynamical abnormalities. Still, the mechanisms and regulatory pathways underlying the interaction between mitophagy and mitochondrial dynamics remain unexplored. Like other existing reviews, we review the molecular structure of proteins involved in mitochondrial dynamics and mitochondrial autophagy, and how their abnormalities can lead to the development of related diseases. We will also review the individual or synergistic effects of abnormal mitochondrial dynamics and mitophagy leading to cellular proliferation, differentiation and invasion. In addition, we explore the mechanisms underlying mitochondrial dynamics and mitochondrial autophagy to contribute to targeted and precise regulation of mitochondrial function. Through the study of abnormal mitochondrial dynamics and mitochondrial autophagy regulation mechanisms, as well as the role of early disease development, effective targets for mitochondrial function regulation can be proposed to enable accurate diagnosis and treatment of the associated disorders.
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