How Can Malnutrition Affect Autophagy in Chronic Heart Failure? Focus and Perspectives

Giovanni Corsetti, Evasio Pasini, Claudia Romano, Carol Chen-Scarabelli, Tiziano M Scarabelli, Vincenzo Flati, Louis Saravolatz, Francesco S Dioguardi

Research output: Contribution to journalReview articlepeer-review


Chronic heart failure (CHF) is a disease with important clinical and socio-economic ramifications. Malnutrition and severe alteration of the protein components of the body (protein disarrangements), common conditions in CHF patients, are independent correlates of heart dysfunction, disease progression, and mortality. Autophagy, a prominent occurrence in the heart of patients with advanced CHF, is a self-digestive process that prolongs myocardial cell lifespan by the removal of cytosolic components, such as aging organelles and proteins, and recycles the constituent elements for new protein synthesis. However, in specific conditions, excessive activation of autophagy can lead to the destruction of molecules and organelles essential to cell survival, ultimately leading to organ failure and patient death. In this review, we aim to describe the experimental and clinical evidence supporting a pathophysiological role of nutrition and autophagy in the progression of CHF. The understanding of the mechanisms underlying the interplay between nutrition and autophagy may have important clinical implications by providing molecular targets for innovative therapeutic strategies in CHF patients.

Original languageEnglish
Pages (from-to)3332
Number of pages12
JournalInt J Mol Sci
Issue number7
Publication statusPublished - Mar 24 2021


  • Animals
  • Autophagy
  • Cell Survival
  • Chronic Disease
  • Cytosol/metabolism
  • Disease Progression
  • Heart/physiology
  • Heart Failure/complications
  • Humans
  • Malnutrition/complications
  • Metabolism
  • Mice
  • Muscle, Skeletal/metabolism
  • Myocardial Contraction
  • Myocardium/metabolism
  • Myocytes, Cardiac/metabolism
  • Rats
  • Risk Assessment
  • TOR Serine-Threonine Kinases/metabolism


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