Editorial Volume 15, Issue 9 pp 3223—3225

Figure 1. Pathophysiological contribution of dicarbonyl stress to mitochondrial dysfunction in the heart during aging through the glycation of RyR and FoF1-ATP synthase. Accumulation of dicarbonyl compounds is favored by the reduction in the efficiency of glyoxalase-dependent detoxification system. This mechanism underlies an energy supply/demand mismatch in the aging cardiomyocytes, favoring the transition towards a failing phenotype, and increases cells’ susceptibility to undergo mPTP and death during I/R injury. Abbreviations: Glo-1: glyoxalase 1; RyR: ryanodine receptor; SR: sarcoplasmic reticulum; mPTP: mitochondrial permeability transition pore; HF: heart failure; I/R: ischemia/reperfusion.