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