کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2190473 1550411 2016 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Receptor-mediated mitophagy
ترجمه فارسی عنوان
میتوفیگی میانجی گیرنده
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
چکیده انگلیسی


• Mitochondrial elimination is mediated through mitophagy.
• Mitophagy is important for maintaining cellular and organ homeostasis.
• Receptors on the outer mitochondrial membrane play an important role in mitophagy.
• BCL2L13 has roles both in mitochondrial fission and as a mitophagy receptor.

Mitochondria are essential organelles that supply ATP through oxidative phosphorylation to maintain cellular homeostasis. Extrinsic or intrinsic agents can impair mitochondria, and these impaired mitochondria can generate reactive oxygen species (ROS) as byproducts, inducing cellular damage and cell death. The quality control of mitochondria is essential for the maintenance of normal cellular functions, particularly in cardiomyocytes, because they are terminally differentiated. Accumulation of damaged mitochondria is characteristic of various diseases, including heart failure, neurodegenerative disease, and aging-related diseases. Mitochondria are generally degraded through autophagy, an intracellular degradation system that is conserved from yeast to mammals. Autophagy is thought to be a nonselective degradation process in which cytoplasmic proteins and organelles are engulfed by isolation membrane to form autophagosomes in eukaryotic cells. However, recent studies have described the process of selective autophagy, which targets specific proteins or organelles such as mitochondria. Mitochondria-specific autophagy is called mitophagy. Dysregulation of mitophagy is implicated in the development of chronic diseases including neurodegenerative diseases, metabolic diseases, and heart failure. In this review, we discuss recent progress in research on mitophagy receptors.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 95, June 2016, Pages 50–56
نویسندگان
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