Dialogue between endoplasmic reticulum and mitochondria as a key actor of vascular dysfunction associated to metabolic disorders.

Metabolic syndrome due to its association with increased risk of cardiovascular diseases and cardiac mortality, comprises a cluster of metabolic abnormalities such as central obesity, hyperglycemia, dyslipidemia, and hypertension. Recent studies have shown that metabolic syndrome patients exhibit impaired nitric oxide-mediated vasodilatation leading to endothelial dysfunction in addition to insulin resistance. Interestingly, development and maintenance of the unfolded protein response of the endoplasmic reticulum stress revealed a surprisingly direct link with metabolic syndrome and endothelial dysfunction. On the other hand, in metabolic disorders, interaction between endoplasmic reticulum and mitochondria is mandatory for the generation of mitochondrial oxidative stress and perturbation of mitochondrial function accounting, at least in part, for vascular dysfunction. Herein, we review the impact of the dialogue between endoplasmic reticulum and mitochondria in modulating the cellular signals governing vascular alterations associated to metabolic disorders.