| Autor: |
Seng, Crystal, Pearce, Luke, Meizoso-Huesca, Aldo, Singh, Daniel P., Murphy, Robyn M., Lamboley, Cedric R., Launikonis, Bradley S. |
| Předmět: |
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| Zdroj: |
American Journal of Physiology: Cell Physiology; Oct2022, Vol. 323 Issue 4, pC1285-C1289, 5p |
| Abstrakt: |
Ca2+ is an integral component of the functional and developmental regulation of the mitochondria. In skeletal muscle, Ca2+ is reported to modulate the rate of ATP resynthesis, regulate the expression of peroxisome proliferator-activated receptor-gamma coactivator 1 (PGC1a) following exercise, and drive the generation of reactive oxygen species (ROS). Due to the latter, mitochondrial Ca2+ overload is recognized as a pathophysiological event but the former events represent important physiological functions in need of tight regulation. Recently, we described the relationship between [Ca2+]mito and resting [Ca2+]cyto and other mitochondrial Ca2+-handling properties of skeletal muscle. An important next step is to understand the triggers for Ca2+ redistribution between intracellular compartments, which determine the mitochondrial Ca2+ load. These triggers in both physiological and pathophysiological scenarios can be traced to the coupled activity of the ryanodine receptor 1 (RyR1) and store-operated Ca2+ entry (SOCE) in the resting muscle. In this piece, we will discuss some issues regarding Ca2+ measurements relevant to mitochondrial Ca2+-handling, the steady-state relationship between cytoplasmic and mitochondrial Ca2+, and the potential implications for Ca2+ handling by muscle mitochondria and cellular function. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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