Key result
This review highlights novel molecular maladaptive mechanisms, including mitochondrial energetic dysfunction, calcium handling, and O-GlcNAcylation, that trigger cardiac disease in aging and metabolic syndrome.
This review highlights molecular mechanisms, including mitochondrial dysfunction and O-GlcNAcylation, linking metabolic syndrome and aging in the heart.
Should not change clinical management of cardiac disease in metabolic syndrome; leaves open targeted mechanistic validation.
Risk factors that define the metabolic syndrome (MetS) develop with age increasing its prevalence. Therefore, MetS can be considered an age-related health problem. Mechanism involved in aging and MetS are incompletely understood. The goal of this review is to highlight novel molecular maladaptive mechanism that tiger cardiac disease and common in aging and MetS. We focus on mitochondrial energetic function as well as mitochondrial calcium handling. In addition, we analyzed the role of O-GlcNAcylation which is a posttranslational modification that triggers multiple signaling pathways.
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Juarez et al. (2017) conducted a review in Metabolic syndrome and aging heart. Molecular mechanisms (mitochondrial energetic function, calcium handling, O-GlcNAcylation) was evaluated. This review highlights novel molecular maladaptive mechanisms, including mitochondrial energetic dysfunction, calcium handling, and O-GlcNAcylation, that trigger cardiac disease in aging and metabolic syndrome.
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