Inositol 1,4,5-trisphosphate-mediated sarcoplasmic reticulum-mitochondrial crosstalk influences adenosine triphosphate production via mitochondrial Ca2+ uptake through the mitochondrial ryanodine receptor in cardiac myocytes

摘要

Elevated levels of inositol 1,4,5-trisphosphate (IP3) in adult cardiac myocytes are typically associated with the development of cardiac hypertrophy, arrhythmias, and heart failure. IP3 enhances intracellular Ca2+ release via IP3 receptors (IP(3)Rs) located at the sarcoplasmic reticulum (SR). We aimed to determine whether IP3-induced Ca2+ release affects mitochondrial function and determine the underlying mechanisms.