Glycative damage to the ryanodine receptor (RyR2) is identified as a mechanistic driver of sarcoplasmic reticulum calcium leak and subsequent mitochondrial damage in the aging heart.
Mitochondria from aging hearts develop calcium overload secondary to SR calcium leak. Glycative damage of RyR2, favored by deficient dicarbonyl detoxification capacity, contributes to calcium leak and mitochondrial damage in the senescent myocardium.
Ruiz‐Meana et al. (Thu,) studied this question.
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