Mitochondrial Ca2+ levels lower down rate of metabolic diseases and cardiomyopathies

Mitochondrial is an important cell organelle that generates ATP that is used as sole energy molecule for all physiological and metabolic activities. It supplies cellular energy and assist in signaling, cell metabolism, cellular differentiation, cell survival and other cell-specific functions. Calcium uptake takes place through mitochondrial outer membrane by voltage-dependent anion channels. After formation of electrochemical gradient and equilibrium on both sides’ mitochondrial functions become normal. It is maintained during oxidative phosphorylation. Thus buffering of cytosolic Ca2+ levels regulate mitochondrial effector functions. Ca2+ transported into mitochondria regulates its metabolism and causes transient depolarisation of mitochondrial membrane. Imbalance in Ca2+ levels cause cardiac myocyte injury that is increased with the decline in pH.1 Dysregulated mitochondrial Ca2+ level and its imbalances generate ischemia neurodegenerative diseases, neuropsychiatric disorders and cancer.2 Accumulation of extra calcium in mitochondria also increases production and modulation of reactive oxygen species. Therefore, balanced Ca2+ buffering is required for normal mitochondrial functions, cell survival and longevity. Mitochondria also involve in control of cell cycle and cell growth. Hence, excessive calcium influx increases ROS generation, induces mitochondrial depolarization and triggers sever pathogenesis. Contrary to this low calcium level affects homoeostasis and redox signaling.3 It also gives rise stress particularly, nitrosative or oxidative stress. More often, excessive calcium uptake of calcium and accumulation of it in cardiac muscle cells result in mitochondrial dysfunctions that impose heart disease. Mitochondria play a central role in cell life and cell death. Availability of Ca2+ in cell from endoplasmic reticulum plays a pivotal role in cell proliferation.