Cell death regulation by MAMs: from molecular mechanisms to therapeutic implications in cardiovascular diseases
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2022Metadata
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Li, Yiran E.
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Cell death regulation by MAMs: from molecular mechanisms to therapeutic implications in cardiovascular diseases
Abstract
The endoplasmic reticulum (ER) and mitochondria are interconnected intracellular organelles with vital roles in the regulation of cell signaling and function. While the ER participates in a number of biological processes including lipid biosynthesis, Ca2+ storage and protein folding and processing, mitochondria are highly dynamic organelles governing ATP synthesis, free radical production, innate immunity and apoptosis. Interplay between the ER and mitochondria plays a crucial role in regulating energy metabolism and cell fate control under stress. The mitochondria-associated membranes (MAMs) denote physical contact sites between ER and mitochondria that mediate bidirectional communications between the two organelles. Although Ca2+ transport from ER to mitochondria is vital for mitochondrial homeostasis and energy metabolism, unrestrained Ca2+ transfer may result in mitochondrial Ca2+ overload, mitochondrial damage and cell death. Here we summarize the roles of MAMs in cell physiology and its impact in pathological conditions with a focus on cardiovascular disease. The possibility of manipulating ER-mitochondria contacts as potential therapeutic approaches is also discussed.
Patrocinador
National Key R&D Program of China 2017YFA0506000
United States Department of Defense
Air Force Office of Scientific Research (AFOSR) FA9550-16-1-0384
Comision Nacional de Investigacion Cientifica y Tecnologica (CONICYT)
CONICYT FONDAP 15150012
Takeda Pharmaceutical Company Ltd P09-015-F
United States Department of Defense W81XWH2110960
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Cell Death and Disease (2022) 13:504
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