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Mitochondrial complex I deficiency and cardiovascular diseases: current evidence and future directions

Authors
  • Forte, Maurizio1
  • Palmerio, Silvia1
  • Bianchi, Franca1
  • Volpe, Massimo1, 2
  • Rubattu, Speranza1, 2
  • 1 IRCCS Neuromed, Department of Angiocardioneurology, Località Camerelle, Pozzilli, IS, 86077, Italy , Pozzilli (Italy)
  • 2 Sapienza University of Rome, Ospedale S. Andrea, Department of Clinical and Molecular Medicine, School of Medicine and Psychology, Rome, Italy , Rome (Italy)
Type
Published Article
Journal
Journal of Molecular Medicine
Publisher
Springer-Verlag
Publication Date
Mar 12, 2019
Volume
97
Issue
5
Pages
579–591
Identifiers
DOI: 10.1007/s00109-019-01771-3
Source
Springer Nature
Keywords
License
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Abstract

Compelling evidence demonstrates the emerging role of mitochondrial complex I deficiency in the onset and development of cardiovascular diseases (CVDs). In particular, defects in single subunits of mitochondrial complex I have been associated with cardiac hypertrophy, ischemia/reperfusion injury, as well as diabetic complications and stroke in pre-clinical studies. Moreover, data obtained in humans revealed that genes coding for complex I proteins were associated with different CVDs. In this review, we discuss recent experimental studies that underline the contributory role of mitochondrial complex I deficiency in the etiopathogenesis of several CVDs, with a particular focus on those involving loss of function models of mitochondrial complex I. We also discuss human studies and potential therapeutic strategies able to rescue mitochondrial function in CVDs.

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