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Table 1 The role of mitochondrial Ca2+ homeostasis in cellular functions

From: Role of mitochondrial dysfunction and dysregulation of Ca2+ homeostasis in the pathophysiology of insulin resistance and type 2 diabetes

Study subjects Manipulation of mitochondrial Ca2+ ions Observations Ref.
 In vitro
  Human
   HeLa cells knockdown of MCU increase of mitochondrial Ca2+ [40]
increase of ROS [40]
decrease of SOCE response [43]
   Lung cells knockdown of MCU decrease of inflammasome activation [44]
decrease of ROS [44]
   Skin fibroblasts point mutation of MICU1 decrease of maximal OCR [47]
increase of mitochondrial Ca2+ uptake [47]
   HEK cells C-terminal deletion of EMRE increase of mitochondrial Ca2+ [35]
   Hepatocytes knockdown of MAMs components (IP3R, VDAC, GRP75) decrease of insulin signaling [69]
 Rat    
   Beta cells knockdown of MCU or MICU1 decrease of mitochondrial Ca2+ [41]
decrease of glucose-stimulated insulin secretion [41]
   Leukemia cells knockdown of MCU decrease of SOCE response [42]
decrease of mitochondrial Ca2+ uptake [42]
   Cardiomyocytes overexpression of TFAM increase of mitochondrial Ca2+ [61]
increase of ATP production [61]
increase of SERCA expression [61]
 Mouse
   Adipocytes downregulation of TFAM, PGC-1α decrease of mitochondrial Ca2+ [62]
increase of ROS [62]
decrease of insulin-stimulated glucose uptake [62]
 In vivo
  Mouse
   Skeletal muscle knockout of MCU decrease of mitochondrial Ca2+ uptake [39]
decrease of maximal OCR [39]
decrease of PDH activity [39, 46]
decrease of muscle function [39]
decrease of muscle size [46]
defects in mitochondrial morphology [46]
   Heart overexpression of DN-MCU decrease of maximal OCR [45]
decrease of heart rate upon stimulation [45]
   Adipose tissue knockdown of MAMs components (Cisd2) glucose intolerance [60]
decrease of maximal OCR [60]
decrease of mitochondrial Ca2+ uptake [60]
   Liver knockout of MICU1 increase of mitochondrial Ca2+ [48]
increase of ROS [48]
decrease of ATP [48]
defects in mitochondrial morphology [48]
knockdown of MICU1 impaired liver regeneration [49]
inflexibility of MAM structure decrease of maximal OCR [72]
decrease of glucose infusion rate [72]
glucose intolerance [72]
knockdown of MAMs components (CypD) hepatic insulin resistance [69]