Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 7, Pages -Publisher
MDPI
DOI: 10.3390/ijms22073332
Keywords
malnutrition; autophagy; heart failure; chronic diseases; amino acids
Funding
- Dolomite-Franchi S.p.a. (Marone, Brescia, Italy)
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Chronic heart failure is a disease with significant clinical and socio-economic implications, often accompanied by malnutrition and protein disarrangements. Autophagy plays a crucial role in disease progression, with excessive activation potentially leading to cell death and organ failure in patients. Understanding the interplay between nutrition and autophagy could provide important molecular targets for innovative therapeutic strategies in CHF patients.
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.
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