The roles of autophagy in vascular smooth muscle cells

Tai, Shi; Hu, Xinqun; Peng, Daoquan; Zhou, Shenghua; Zheng, Xi-Long

doi:10.1016/j.ijcard.2016.02.128

Cited by 73 publications

(51 citation statements)

References 90 publications

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“…LAMP2A and cathepsin D deficiencies are also known causes of cardiomyopathies, and impaired autophagy can promote atherosclerosis by promoting VSMC senescence and cell death 126,127 . Protein aggregation has also been implicated in T2D, as it has been found that amylin aggregates form in the pancreas in T2D mouse models; furthermore, aggregation is increased by genetic ablation of the autophagic protein ATG7 (REF.…”

Section: Proteostasis and Proteolysismentioning

confidence: 99%

Shared molecular and cellular mechanisms of premature ageing and ageing-associated diseases

Kubben

Misteli

2017

Nat Rev Mol Cell Biol

246

203

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Ageing is the predominant risk factor for many common diseases. Human premature ageing diseases are powerful model systems to identify and characterize cellular mechanisms that underpin physiological ageing. Their study also leads to a better understanding of the causes, drivers and potential therapeutic strategies of common diseases associated with ageing, including neurological disorders, diabetes, cardiovascular diseases and cancer. Using the rare premature ageing disorder Hutchinson–Gilford progeria syndrome as a paradigm, we discuss here the shared mechanisms between premature ageing and ageing-associated diseases, including defects in genetic, epigenetic and metabolic pathways; mitochondrial and protein homeostasis; cell cycle; and stem cell-regenerative capacity.

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Section: Proteostasis and Proteolysismentioning

confidence: 99%

Shared molecular and cellular mechanisms of premature ageing and ageing-associated diseases

Kubben

Misteli

2017

Nat Rev Mol Cell Biol

246

203

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“…Additionally, lipophagy may play a role in the hydrolysis of stored cholesterol droplets in macrophages, thereby facilitating cholesterol efflux and reducing atherosclerotic lipid accumulation [84]. Autophagy is also activated in VSMCs in vascular disease, which is important for VSMC survival and plasticity [85]. Grootaert et al demonstrated that defective autophagy in VSMCs promotes senescence, ligation-induced neointima formation and diet-induced atherogenesis and prevents oxidative stress-induced cell death [86].…”

Section: Introductionmentioning

confidence: 99%

The protective role of Sirt1 in vascular tissue: its relationship to vascular aging and atherosclerosis

Kitada

Ogura

Koya

2016

Aging

216

149

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Cardiovascular disease (CVD) due to atherosclerosis is the main cause of death in both the elderly and patients with metabolic diseases, including diabetes. Aging processes contribute to the pathogenesis of atherosclerosis. Calorie restriction (CR) is recognized as a dietary intervention for promoting longevity and delaying age-related diseases, including atherosclerosis. Sirt1, an NAD+-dependent deacetylase, is considered an anti-aging molecule and is induced during CR. Sirt1 deacetylates target proteins and is linked to cellular metabolism, the redox state and survival pathways. Sirt1 expression/activation is decreased in vascular tissue undergoing senescence. Sirt1 deficiency in endothelial cells (ECs), vascular smooth muscle cells (VSMCs) and monocytes/macrophages contributes to increased oxidative stress, inflammation, foam cell formation, senescences impaired nitric oxide production and autophagy, thereby promoting vascular aging and atherosclerosis. Endothelial dysfunction, activation of monocytes/macrophages, and the functional and phenotypical plasticity of VSMCs are critically implicated in the pathogenesis of atherosclerosis through multiple mechanisms. Therefore, the activation of Sirt1 in vascular tissue, which includes ECs, monocytes/macrophages and VSMCs, may be a new therapeutic strategy against atherosclerosis and the increasing resistance to the metabolic disorder-related causal factors of CVD. In this review, we discuss the protective role of Sirt1 in the pathophysiology of vascular aging and atherosclerosis.

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“…However, autophagy activity is greatly up-regulated in response to nutrient limitation or to an altered intracellular milieu. A dysregulation of autophagy activity contributes to the pathology of multiple diseases (Chang et al 2015;Tai et al 2016;Edens et al 2016), including complications of pregnancy (Hung et al 2012;Kanninen at el. 2013b;Gao et al 2015;Brickle et al 2015;Agrawal et al 2015).…”

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confidence: 99%

The influence of oxidative stress and autophagy cross regulation on pregnancy outcome

Ramos

2016

Cell Stress and Chaperones

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The generation of reactive oxygen species (ROS), a byproduct of aerobic energy metabolism, is maintained at physiological levels by the activity of antioxidant components. Insufficiently opposed ROS results in oxidative stress characterized by altered mitochondrial function, decreased protein activity, damage to nucleic acids, and induction of apoptosis. Elevated levels of inadequately opposed ROS induce autophagy, a major intracellular pathway that sequesters and removes damaged macromolecules and organelles. In early pregnancy, autophagy induction preserves trophoblast function in the low oxygen and nutrient placental environment. Inadequate regulation of the ROS-autophagy axis leads to abnormal autophagy activity and contributes to the development of preeclampsia and intrauterine growth restriction. ROS-autophagy interactions are altered at the end of gestation and participate in the initiation of parturition at term. The induction of high levels of ROS coupled with a failure to induce a corresponding increase in autophagy results in the triggering of preterm labor and delivery.Keywords Oxidative stress . Autophagy . Preeclampsia . Intrauterine growth restriction . Preterm birth . PregnancyReactive oxygen species (ROS), such as superoxide radicals, hydroxyl radicals, alkoxy radicals as well as the non-radical intermediates hydrogen peroxide, ozone, and singlet oxygen, are byproducts of aerobic energy metabolism (Sies 1991;Finkel 2011). The concentration of these radicals is maintained at physiological levels by activity of the antioxidant enzymes superoxide dismutase, catalase, and peroxiredoxins as well as by concentrations of glutathione and vitamins C and E. When this system becomes out of balance, the generation of insufficiently opposed ROS results in altered mitochondrial function, a diminution of protein activity, damage to nucleic acids, and induction of apoptosis. The consequent tissue damage is manifested in a range of pathologies to different organ systems (Domingueti et al. 2015;Aluganti et al. 2016;Hernández et al. 2016). Recently, insufficiently regulated ROS has been recognized as a major contributor to disorders of pregnancy (Coppe et al. 2010;Redman and Sargent 2010;Menon 2014; Wu et al. 2015a, b;Zhang et al. 2015).A major pathway for removing macromolecules and organelles that have been damaged by ROS is macroautophagy, hereafter referred to as autophagy. This catabolic process is responsible for eliminating altered proteins, mitochondria, and inflammasomes from the cytoplasm. Macromolecules and organelles marked for destruction are enclosed within a doublemembrane structure called autophagosome. Its subsequent fusion with a lysosome results in degradation of the enclosed entity and release of the component amino acids, carbohydrates, nucleic acid degradation products, and lipids into the cytoplasm as building blocks for synthesis of new macromolecules or for the generation of energy by mitochondria. Autophagy is a constitutive process and functions at a low level under physiologica...

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The roles of autophagy in vascular smooth muscle cells

Cited by 73 publications

References 90 publications

Shared molecular and cellular mechanisms of premature ageing and ageing-associated diseases

Shared molecular and cellular mechanisms of premature ageing and ageing-associated diseases

The protective role of Sirt1 in vascular tissue: its relationship to vascular aging and atherosclerosis

The influence of oxidative stress and autophagy cross regulation on pregnancy outcome

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