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The interplay between mitochondria and store-operated Ca2+ entry: Emerging insights into cardiac diseases |
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| Authors: | Jinliang Nan Jiamin Li Yinuo Lin Muhammad Saif Ur Rahman Zhengzheng Li Lingjun Zhu |
| Institution: | 1. Provincial Key Cardiovascular Research Laboratory, Department of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Zhejiang Province, Hangzhou, China
Contribution: Conceptualization (lead), Writing - original draft (equal);2. Provincial Key Cardiovascular Research Laboratory, Department of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Zhejiang Province, Hangzhou, China Contribution: Writing - original draft (equal);3. Wenzhou Municipal Key Cardiovascular Research Laboratory, Department of Cardiology, The First Affiliated Hospital, Wenzhou Medical University, Zhejiang Province, Wenzhou, China Contribution: Writing - review & editing (equal);4. Zhejiang University-University of Edinburgh Biomedical Institute, Haining, Zhejiang, China Clinical Research Center, The Second Affiliated Hospital Zhejiang University School of Medicine, Hangzhou, China;5. Department of Neurology, Research Institute of Experimental Neurobiology, The First Affiliated Hospital, Wenzhou Medical University, Zhejiang Province, Wenzhou, China Contribution: Writing - review & editing (equal);6. Provincial Key Cardiovascular Research Laboratory, Department of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Zhejiang Province, Hangzhou, China |
| Abstract: | Store-operated Ca2+ entry (SOCE) machinery, including Orai channels, TRPCs, and STIM1, is key to cellular calcium homeostasis. The following characteristics of mitochondria are involved in the physiological and pathological regulation of cells: mitochondria mediate calcium uptake through calcium uniporters; mitochondria are regulated by mitochondrial dynamic related proteins (OPA1, MFN1/2, and DRP1) and form mitochondrial networks through continuous fission and fusion; mitochondria supply NADH to the electron transport chain through the Krebs cycle to produce ATP; under stress, mitochondria will produce excessive reactive oxygen species to regulate mitochondria-endoplasmic reticulum interactions and the related signalling pathways. Both SOCE and mitochondria play critical roles in mediating cardiac hypertrophy, diabetic cardiomyopathy, and cardiac ischaemia-reperfusion injury. All the mitochondrial characteristics mentioned above are determinants of SOCE activity, and vice versa. Ca2+ signalling dictates the reciprocal regulation between mitochondria and SOCE under the specific pathological conditions of cardiomyocytes. The coupling of mitochondria and SOCE is essential for various pathophysiological processes in the heart. Herein, we review the research focussing on the reciprocal regulation between mitochondria and SOCE and provide potential interplay patterns in cardiac diseases. |
| Keywords: | cardiac hypertrophy diabetic cardiomyopathy endoplasmic reticulum ischaemia-reperfusion injury mitochondria store-operated Ca2+ entry |