Disturbed cardiac mitochondrial and cytosolic calcium handling in a metabolic risk‐related rat model of heart failure with preserved ejection fraction

Abstract

The free mitochondrial calcium concentration is higher in HFpEF owing to alterations in mitochondrial and cytosolic Ca²⁺ handling. This coupling between cytosolic and mitochondrial Ca²⁺ levels may compensate for myocardial ATP supply in vivo under conditions of mild mitochondrial dysfunction. However, if mitochondrial Ca²⁺ concentration is sustainedly increased, it might trigger mitochondrial permeability transition pore opening.