Mitophagy: At the heart of mitochondrial quality control in cardiac aging and frailty

Anna Picca, Riccardo Calvani, Hélio José Coelho-Júnior, Emanuele Marzetti

Risultato della ricerca: Contributo in rivistaArticolo in rivista


Cardiovascular disease is highly prevalent among older adults and poses a huge burden on morbidity, disability, and mortality. The age-related increased vulnerability of the cardiovascular system towards stressors is a pathophysiological trait of cardiovascular disease. This has been associated with a progressive deterioration of blood vessels and decline in heart function during aging. Cardiomyocytes rely mostly on oxidative metabolism for deploying their activities and mitochondrial metabolism is crucial to this purpose. Dysmorphic, inefficient, and oxidant-producing mitochondria have been identified in aged cardiomyocytes in association with cardiac structural and functional alterations. These aberrant organelles are thought to arise from inefficient mitochondrial quality control, which has therefore been place in the spotlight as a relevant mechanism of cardiac aging. As a result of alterations in mitochondrial quality control and redox dyshomeostasis, mitochondrial damage accumulates and contributes to cardiac frailty. Herein, we discuss the contribution of defective mitochondrial quality control pathways to cardiac frailty. Emerging findings pointing towards the exploitation of these pathways as therapeutic targets against cardiac aging and cardiovascular disease will also be illustrated.
Lingua originaleEnglish
pagine (da-a)1-9
Numero di pagine9
RivistaExperimental Gerontology
Stato di pubblicazionePubblicato - 2021


  • Aged
  • Aging
  • Autophagy
  • Cardioprotection
  • Extracellular vesicles
  • Frailty
  • Humans
  • Mitochondria
  • Mitochondrial derived vesicles
  • Mitochondrial quality control
  • Mitophagy
  • Myocytes, Cardiac
  • Therapeutics


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