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线粒体自噬调控中的钙稳态

Calcium Homeostasis in the Control of Mitophagy.

作者信息

Perrone Mariasole, Patergnani Simone, Di Mambro Tommaso, Palumbo Laura, Wieckowski Mariusz R, Giorgi Carlotta, Pinton Paolo

机构信息

Department of Medical Sciences, Section of Experimental Medicine and Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy.

Laboratory of Mitochondrial Biology and Metabolism, Nencki Institute of Experimental Biology of the Polish Academy of Sciences, Warsaw, Poland.

出版信息

Antioxid Redox Signal. 2023 Mar;38(7-9):581-598. doi: 10.1089/ars.2022.0122. Epub 2023 Mar 1.

Abstract

Maintenance of mitochondrial quality is essential for cellular homeostasis. Among processes responsible for preserving healthy mitochondria, mitophagy selectively eliminates dysfunctional mitochondria by targeting them to the autophagosome for degradation. Alterations in mitophagy lead to the accumulation of damaged mitochondria, which plays an essential role in several diseases such as carcinogenesis and tumor progression, neurodegenerative disorders, and autoimmune and cardiovascular pathologies. Calcium (Ca) plays a fundamental role in cell life, modulating several pathways, such as gene expression, proliferation, differentiation, metabolism, cell death, and survival. Indeed, because it is involved in all these events, Ca is the most versatile intracellular second messenger. Being a process that limits cellular degeneration, mitophagy participates in cellular fate decisions. Several mitochondrial parameters, such as membrane potential, structure, and reactive oxygen species, can trigger the activation of mitophagic machinery. These parameters regulate not only mitophagy but also the mitochondrial Ca uptake. Ca handling is fundamental in regulating ATP production by mitochondria and mitochondrial quality control processes. Despite the growing literature about the link between Ca and mitophagy, the mechanism by which Ca homeostasis regulates mitophagy is still debated. Several studies have revealed that excessive mitophagy together with altered mitochondrial Ca uptake leads to different dysfunctions in numerous diseases. Thus, therapeutic modulation of these pathways is considered a promising treatment. . 38, 581-598.

摘要

线粒体质量的维持对于细胞内稳态至关重要。在负责维持健康线粒体的过程中,线粒体自噬通过将功能失调的线粒体靶向自噬体进行降解,从而选择性地清除它们。线粒体自噬的改变会导致受损线粒体的积累,这在多种疾病中起着重要作用,如癌症发生和肿瘤进展、神经退行性疾病以及自身免疫和心血管疾病。钙(Ca)在细胞生命中起着基础性作用,调节多种途径,如基因表达、增殖、分化、代谢、细胞死亡和存活。事实上,由于钙参与了所有这些事件,它是最通用的细胞内第二信使。作为一个限制细胞退化的过程,线粒体自噬参与细胞命运的决定。几个线粒体参数,如膜电位、结构和活性氧物种,可以触发线粒体自噬机制的激活。这些参数不仅调节线粒体自噬,还调节线粒体对钙的摄取。钙的处理在调节线粒体产生ATP和线粒体质量控制过程中至关重要。尽管关于钙和线粒体自噬之间联系的文献越来越多,但钙稳态调节线粒体自噬的机制仍存在争议。几项研究表明,过度的线粒体自噬以及线粒体钙摄取的改变会在多种疾病中导致不同的功能障碍。因此,对这些途径的治疗性调节被认为是一种有前景的治疗方法。. 38, 581 - 598。

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