Autophagy and cardiovascular aging

Nair, Sreejayan; Ren, Jun

doi:10.4161/cc.20317

Cited by 66 publications

(33 citation statements)

References 98 publications

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“…The functional relationship among the three types of autophagy remains largely undefined but crosstalk among them may exist as CMA has been found to be constitutively activated in cells with impaired macroautophagy [53]. Microautophagy and CMA have rarely been studied in cardiac pathogenesis but research into the involvement of macroautophagy (hereafter referred to as autophagy) in cardiac physiology and pathology has exploded in the past decade [54, 55]. …”

Section: Autophagy Protects Against Cardiac Proteotoxicitymentioning

confidence: 99%

The interplay between autophagy and the ubiquitin–proteasome system in cardiac proteotoxicity

Wang

2015

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Proteotoxicity refers to the detrimental effects of damaged/misfolded proteins on the cell. Cardiac muscle is particularly susceptible to proteotoxicity because sustained and severe proteotoxic stress leads to cell death and cardiac muscle has very limited self-renewal capacity. The ubiquitin-proteasome system (UPS) and the autophagic-lysosomal pathway (ALP) are two major pathways responsible for degradation of most cellular proteins. Alterations of UPS and ALP functions are associated with the accumulation of proteotoxic species in the heart, a key pathological feature of common forms of heart disease including idiopathic, ischemic, and pressure-overloaded cardiomyopathies and a large subset of congestive heart failure. Emerging evidence suggests proteasome inhibition or impairment activates autophagy and conversely, acute ALP inhibition may sometimes increase intrinsic proteasome peptidase activities but chronic ALP inhibition hinders UPS performance in ubiquitinated protein degradation. The exact molecular basis on which the two degradative pathways interact remains largely undefined. Here we review current understanding of the roles of the UPS and autophagy in the control of cardiac proteotoxicity, with a specific focus on the crosstalk between the two pathways.

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Section: Autophagy Protects Against Cardiac Proteotoxicitymentioning

confidence: 99%

The interplay between autophagy and the ubiquitin–proteasome system in cardiac proteotoxicity

Wang

2015

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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“…16,17 Abnormal autophagy is implicated in multiple tissues of obesity; 18 for instance, autophagosome formation is enhanced in pancreatic β cells and adipose tissue in obese mice, and enhanced autophagy was observed in advanced glycation end products (AGEs)-induced early injury of human umbilical vein endothelial cells and the process of AGEsinduced proliferation of VSMCs. 19,20 On the other hand, ER stress could trigger autophagic imbalance and defective insulin signaling in mammalian cells.…”

Section: Introductionmentioning

confidence: 99%

Intermittent injections of osteocalcin reverse autophagic dysfunction and endoplasmic reticulum stress resulting from diet-induced obesity in the vascular tissue via the NFκB-p65-dependent mechanism

Zhou¹,

Li²,

Liu³

et al. 2013

Cell Cycle

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“…Indeed, given that autophagy is involved in the prevention of different human pathological conditions, including heart and liver disease, cancer, neurodegeneration, as well as infectious and metabolic disorders, 4-6 the development of highly specific autophagy modulators has become a major clinical priority. Along these lines, it is noteworthy that autophagy plays an essential role in embryogenesis, 7 aging, 8 regulation of blood glucose and amino acids, 9 thrombosis, 10 and lipid metabolism. 11 Systemic or tissue-specific deletion of autophagyrelated (Atg) genes in various organisms, including mice, may lead to serious malformations and even death, 12 supporting the general hypothesis that autophagy is an essential process that contributes to health and overall well-being.…”

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confidence: 99%

Autophagy in Vascular Disease

Meyer

Grootaert

Michiels

et al. 2015

Circulation Research

243

179

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A utophagy is a complex intracellular process that delivers cytoplasmic constituents for degradation into lysosomes.1,2 Three main types of autophagy have been described: (1) microautophagy, comprising direct engulfment of cytoplasmic material by lysosomes via inward invaginations of the lysosomal membrane, (2) macroautophagy, characterized by formation of double-membrane sequestering compartments termed autophagosomes that fuse with lysosomes for delivery of cytoplasmic cargo, and (3) chaperone-mediated autophagy, mediated by a chaperone complex and lysosomal-associated membrane protein type 2A to degrade cytosolic proteins with a specific targeting motif. The term autophagy usually refers to macroautophagy, which is the most prevalent and beststudied form of autophagy. Also in this review, we will focus exclusively on macroautophagy, further cited as autophagy.Autophagy occurs at basal levels in most tissues to allow constitutive turnover of cytosolic components but is stimulated by environmental stress-related signals (eg, nutrient deprivation and oxidative injury) to recycle nutrients and to generate energy for maintenance of cell viability in unfavorable conditions.1 In addition to cellular stress, basal autophagy can be intensified by specific drugs, 3 indicating that the autophagic machinery is a potential therapeutic target for diverse diseases. Indeed, given that autophagy is involved in the prevention

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Autophagy and cardiovascular aging

Cited by 66 publications

References 98 publications

The interplay between autophagy and the ubiquitin–proteasome system in cardiac proteotoxicity

The interplay between autophagy and the ubiquitin–proteasome system in cardiac proteotoxicity

Intermittent injections of osteocalcin reverse autophagic dysfunction and endoplasmic reticulum stress resulting from diet-induced obesity in the vascular tissue via the NFκB-p65-dependent mechanism

Autophagy in Vascular Disease

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