Nutritional status and cardiac autophagy

Abstract

Autophagy is necessary for the degradation of long-lasting proteins and nonfunctional organelles, and is activated to promote cellular survival. However, overactivation of autophagy may deplete essential molecules and organelles responsible for cellular survival. Lifelong calorie restriction by 40% has been shown to increase the cardiac expression of autophagic markers, which suggests that it may have a cardioprotective effect by decreasing oxidative damage brought on by aging and cardiovascular diseases. Although cardiac autophagy is critical to regulating protein quality and maintaining cellular function and survival, increased or excessive autophagy may have deleterious effects on the heart under some circumstances, including pressure overload-induced heart failure. The importance of autophagy has been shown in nutrient supply and preservation of energy in times of limitation, such as ischemia. Some studies have suggested that a transition from obesity to metabolic syndrome may involve progressive changes in myocardial inflammation, mitochondrial dysfunction, fibrosis, apoptosis, and myocardial autophagy.

Keywords: Autophagy; Heart; Nutrition; Obesity; Starvation.

Fig. 1

Regulation of cardiac autophagy and nutritional status, including overnutrition and undernutrition. mTOR, mammalian target of rapamycin; PI3K, phosphoinositide 3-kinase; TSC, tuberous sclerosis complex; AMPK, adenosine monophosphate-activated protein kinase; Sirt1, Sirtuin 1.