Defective mitochondrial biogenesis: A hallmark of the high cardiovascular risk in the metabolic syndrome?

Enzo Nisoli, Emilio Clementi, Michele O. Carruba, Salvador Moncada

Research output: Contribution to journalArticlepeer-review

Abstract

The metabolic syndrome is a group of risk factors of metabolic origin that are accompanied by increased risk for type 2 diabetes mellitus and cardiovascular disease. These risk factors include atherogenic dyslipidemia, elevated blood pressure and plasma glucose, and a prothrombotic and proinflammatory state. The condition is progressive and is exacerbated by physical inactivity, advancing age, hormonal imbalance, and genetic predisposition. The metabolic syndrome is a particularly challenging clinical condition because its complex molecular basis is still largely undefined. Impaired cell metabolism has, however, been suggested as a relevant pathophysiological process underlying several clinical features of the syndrome. In particular, defective oxidative metabolism seems to be involved in visceral fat gain and in the development of insulin resistance in skeletal muscle. This suggests that mitochondrial function may be impaired in the metabolic syndrome and, thus, in the consequent cardiovascular disease. We have recently found that mitochondrial biogenesis and function are enhanced by nitric oxide in various cell types and tissues, including cardiac muscle. Increasing evidence suggests that this mediator acts as a metabolic sensor in cardiomyocytes. This implies that a defective production of nitric oxide might be linked to dysfunction of the cardiomyocyte metabolism. Here we summarize some recent findings and propose a hypothesis for the high cardiovascular risk linked to the metabolic syndrome.

Original languageEnglish
Pages (from-to)795-806
Number of pages12
JournalCirculation Research
Volume100
Issue number6
DOIs
Publication statusPublished - Mar 2007

Keywords

  • Cardiomyocytes
  • Mitochondrial biogenesis
  • Nitric oxide
  • Obesity
  • Peroxisome proliferator-activated receptor-γ coactivator 1α

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

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