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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 Ca(2+ )release via IP3 receptors (IP3Rs) located at the sarcoplasmic reticulum (SR). We aimed to determine whether IP3-induced Ca(2+ )release affects mitochondrial function and determine the underlying mechanisms.

cardiovascular research

Inositol 1,4,5-trisphosphate-mediated sarcoplasmic reticulum–mitochondrial crosstalk influences adenosine triphosphate production via mitochondrial Ca<sup>2+</sup>uptake through the mitochondrial ryanodine receptor in cardiac myocytes

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

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