The Regulatory Roles of Mitochondrial Calcium and the Mitochondrial Calcium Uniporter in Tumor Cells

Mitochondria, as the main site of cellular energy metabolism and the generation of oxygen free radicals, are the key switch for mitochondria-mediated endogenous apoptosis. Ca<sup>2+</sup> is not only an important messenger for cell proliferation, but it is also an indispensable signal fo...

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Main Authors: Linlin Zhang, Jingyi Qi, Xu Zhang, Xiya Zhao, Peng An, Yongting Luo, Junjie Luo
Format: Article
Language:English
Published: MDPI AG 2022-06-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/23/12/6667
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author Linlin Zhang
Jingyi Qi
Xu Zhang
Xiya Zhao
Peng An
Yongting Luo
Junjie Luo
author_facet Linlin Zhang
Jingyi Qi
Xu Zhang
Xiya Zhao
Peng An
Yongting Luo
Junjie Luo
author_sort Linlin Zhang
collection DOAJ
description Mitochondria, as the main site of cellular energy metabolism and the generation of oxygen free radicals, are the key switch for mitochondria-mediated endogenous apoptosis. Ca<sup>2+</sup> is not only an important messenger for cell proliferation, but it is also an indispensable signal for cell death. Ca<sup>2+</sup> participates in and plays a crucial role in the energy metabolism, physiology, and pathology of mitochondria. Mitochondria control the uptake and release of Ca<sup>2+</sup> through channels/transporters, such as the mitochondrial calcium uniporter (MCU), and influence the concentration of Ca<sup>2+</sup> in both mitochondria and cytoplasm, thereby regulating cellular Ca<sup>2+</sup> homeostasis. Mitochondrial Ca<sup>2+</sup> transport-related processes are involved in important biological processes of tumor cells including proliferation, metabolism, and apoptosis. In particular, MCU and its regulatory proteins represent a new era in the study of MCU-mediated mitochondrial Ca<sup>2+</sup> homeostasis in tumors. Through an in-depth analysis of the close correlation between mitochondrial Ca<sup>2+</sup> and energy metabolism, autophagy, and apoptosis of tumor cells, we can provide a valuable reference for further understanding of how mitochondrial Ca<sup>2+</sup> regulation helps diagnosis and therapy.
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spelling doaj.art-3a43d59d115d4a14bbd4a4ac272cdbff2023-11-23T17:04:44ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-06-012312666710.3390/ijms23126667The Regulatory Roles of Mitochondrial Calcium and the Mitochondrial Calcium Uniporter in Tumor CellsLinlin Zhang0Jingyi Qi1Xu Zhang2Xiya Zhao3Peng An4Yongting Luo5Junjie Luo6Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, ChinaKey Laboratory of Precision Nutrition and Food Quality, Department of Nutrition and Health, China Agricultural University, Beijing 100193, ChinaKey Laboratory of Precision Nutrition and Food Quality, Department of Nutrition and Health, China Agricultural University, Beijing 100193, ChinaKey Laboratory of Precision Nutrition and Food Quality, Department of Nutrition and Health, China Agricultural University, Beijing 100193, ChinaKey Laboratory of Precision Nutrition and Food Quality, Department of Nutrition and Health, China Agricultural University, Beijing 100193, ChinaKey Laboratory of Precision Nutrition and Food Quality, Department of Nutrition and Health, China Agricultural University, Beijing 100193, ChinaKey Laboratory of Precision Nutrition and Food Quality, Department of Nutrition and Health, China Agricultural University, Beijing 100193, ChinaMitochondria, as the main site of cellular energy metabolism and the generation of oxygen free radicals, are the key switch for mitochondria-mediated endogenous apoptosis. Ca<sup>2+</sup> is not only an important messenger for cell proliferation, but it is also an indispensable signal for cell death. Ca<sup>2+</sup> participates in and plays a crucial role in the energy metabolism, physiology, and pathology of mitochondria. Mitochondria control the uptake and release of Ca<sup>2+</sup> through channels/transporters, such as the mitochondrial calcium uniporter (MCU), and influence the concentration of Ca<sup>2+</sup> in both mitochondria and cytoplasm, thereby regulating cellular Ca<sup>2+</sup> homeostasis. Mitochondrial Ca<sup>2+</sup> transport-related processes are involved in important biological processes of tumor cells including proliferation, metabolism, and apoptosis. In particular, MCU and its regulatory proteins represent a new era in the study of MCU-mediated mitochondrial Ca<sup>2+</sup> homeostasis in tumors. Through an in-depth analysis of the close correlation between mitochondrial Ca<sup>2+</sup> and energy metabolism, autophagy, and apoptosis of tumor cells, we can provide a valuable reference for further understanding of how mitochondrial Ca<sup>2+</sup> regulation helps diagnosis and therapy.https://www.mdpi.com/1422-0067/23/12/6667mitochondrial calciumcalcium homeostasiscalcium regulationMCUtumor
spellingShingle Linlin Zhang
Jingyi Qi
Xu Zhang
Xiya Zhao
Peng An
Yongting Luo
Junjie Luo
The Regulatory Roles of Mitochondrial Calcium and the Mitochondrial Calcium Uniporter in Tumor Cells
International Journal of Molecular Sciences
mitochondrial calcium
calcium homeostasis
calcium regulation
MCU
tumor
title The Regulatory Roles of Mitochondrial Calcium and the Mitochondrial Calcium Uniporter in Tumor Cells
title_full The Regulatory Roles of Mitochondrial Calcium and the Mitochondrial Calcium Uniporter in Tumor Cells
title_fullStr The Regulatory Roles of Mitochondrial Calcium and the Mitochondrial Calcium Uniporter in Tumor Cells
title_full_unstemmed The Regulatory Roles of Mitochondrial Calcium and the Mitochondrial Calcium Uniporter in Tumor Cells
title_short The Regulatory Roles of Mitochondrial Calcium and the Mitochondrial Calcium Uniporter in Tumor Cells
title_sort regulatory roles of mitochondrial calcium and the mitochondrial calcium uniporter in tumor cells
topic mitochondrial calcium
calcium homeostasis
calcium regulation
MCU
tumor
url https://www.mdpi.com/1422-0067/23/12/6667
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