Oxidized LDLs trigger endoplasmic reticulum stress and autophagy: Prevention by HDLs

Muller, C.; Salvayre, Robert; Nègre‐Salvayre, Anne; Vindis, Cécile

doi:10.4161/auto.7.5.15003

Cited by 53 publications

(42 citation statements)

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“…Transmission electron microscopy of VSMCs in the fibrous cap of experimental or human plaques revealed features of autophagy (97), and Western blot analysis of advanced human plaques showed elevated levels of LC3-II (98). Several autophagy triggers are present within the atherosclerotic plaque, such as inflammatory mediators (99), ROS (100), oxLDL (101,102), TNF-α (99), osteopontin, and AGEs (103,104). In aortic smooth muscle cells (SMCs), increases in LC3 and autophagy were detected during lipid peroxidation (105).…”

Section: Autophagy In Atherosclerosismentioning

confidence: 99%

Autophagy in cardiovascular biology

Lavandero

Chiong

Rothermel³

et al. 2015

J. Clin. Invest.

280

211

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Autophagy in the vascular systemEndothelial cells. Autophagy can be regulated in vascular endothelial cells by compounds circulating in the bloodstream or localized within the subendothelial layer of atherosclerotic plaque. For example, in cultured HUVECs, vitamin D increases beclin 1, a key comCardiovascular disease is the leading cause of death worldwide. As such, there is great interest in identifying novel mechanisms that govern the cardiovascular response to disease-related stress. First described in failing hearts, autophagy within the cardiovascular system has been widely characterized in cardiomyocytes, cardiac fibroblasts, endothelial cells, vascular smooth muscle cells, and macrophages. In all cases, a window of optimal autophagic activity appears to be critical to the maintenance of cardiovascular homeostasis and function; excessive or insufficient levels of autophagic flux can each contribute to heart disease pathogenesis. In this Review, we discuss the potential for targeting autophagy therapeutically and our vision for where this exciting biology may lead in the future.

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Section: Autophagy In Atherosclerosismentioning

confidence: 99%

Autophagy in cardiovascular biology

Lavandero

Chiong

Rothermel³

et al. 2015

J. Clin. Invest.

280

211

View full text Add to dashboard Cite

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“…HDL and its subfractions offer important cytoprotection for endothelial cells in response to different proapoptotic stimuli. Attenuation of endothelial cell apoptosis by HDL involves inhibition of death receptor, mitochondrial, and endoplasmic reticulum signaling pathways (93)(94)(95)(96). Tumor necrosis factor ␣-induced apoptosis via death-receptor signaling is blocked by HDL via inhibition of CPP32-like protease activity (97 ).…”

Section: Antiapoptotic Effectsmentioning

confidence: 99%

The Changing Face of HDL and the Best Way to Measure It

Karathanasis¹,

Freeman

Gordon

et al. 2017

Clinical Chemistry

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BACKGROUND: HDL cholesterol (HDL-C) is a commonly used lipid biomarker for assessing cardiovascular health. While a central focus has been placed on the role of HDL in the reverse cholesterol transport (RCT) process, our appreciation for the other cardioprotective properties of HDL continues to expand with further investigation into the structure and function of HDL and its specific subfractions. The development of novel assays is empowering the research community to assess different aspects of HDL function, which at some point may evolve into new diagnostic tests. CONTENT:This review discusses our current understanding of the formation and maturation of HDL particles via RCT, as well as the newly recognized roles of HDL outside RCT. The antioxidative, antiinflammatory, antiapoptotic, antithrombotic, antiinfective, and vasoprotective effects of HDL are all discussed, as are the related methodologies for assessing these different aspects of HDL function. We elaborate on the importance of protein and lipid composition of HDL in health and disease and highlight potential new diagnostic assays based on these parameters.

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“…Moreover, Western blot analysis of human carotid plaques showed processing of microtubule-associated protein 1 light chain 3 (LC3) into the autophagosome-specific isoform LC3-II, indicating activation of autophagy. 7 Indeed, in vitro studies identified several potential triggers for autophagy that are present in atherosclerotic plaques, such as inflammation, 10,11 reactive oxygen species production, 12 accumulation of oxidized lipoproteins, 13,14 and endoplasmic reticulum stress. 15 Also, hypoxia is a common feature of advanced human atherosclerotic plaques, caused by inadequate vascularization, 16,17 that is associated with nutrient and growth factor deprivation, a well-known condition leading to induction of autophagy.…”

Section: Autophagy In Atherosclerosismentioning

confidence: 99%

Autophagy in Atherosclerosis

Schrijvers

Meyer

Martinet

2011

ATVB

160

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Abstract-Evidence is accumulating that autophagy occurs in advanced atherosclerotic plaques. Although there is an almost relentless discovery of molecules that are involved in autophagy, studies of selective autophagy induction or inhibition using knockout mice are just now beginning to reveal its biological significance. Most likely, autophagy safeguards plaque cells against cellular distress, in particular oxidative injury, by degrading the damaged intracellular material. In this way, autophagy is protective and contributes to cellular recovery in an unfavorable environment. Pharmacological approaches have recently been developed to stabilize vulnerable, rupture-prone lesions through induction of autophagy. This approach has proven to be successful in short-term studies. However, how autophagy induction affects processes such as inflammation remains to be elucidated and is currently under investigation. This review highlights the possibilities for exploiting autophagy as a drug target for plaque stabilization. Key Words: atherosclerosis Ⅲ pharmacology Ⅲ autophagy Ⅲ cell death Ⅲ plaque stabilization A utophagy, or "self eating," refers to a conserved cellular process for the turnover of organelles and proteins that occurs in all eukaryotic cells. 1 It is activated as an adaptive response to environmental stress (eg, nutrient deprivation, hypoxia, oxidative stress, exposure to xenobiotics) to promote cell survival through the recycling of precursors (amino acids, free fatty acids, nucleotides) derived from the degradation of endogenous cellular components. Typical of autophagy is the formation of double-membrane structures, called phagophores, that engulf intracellular material such as protein aggregates, lipid droplets, and complete organelles for degradation (Figure 1). The phagophore expands and, on completion, forms an autophagosome, which then fuses with lysosomes, thereby generating an autophagolysosome. 2 Incorporation of the outer autophagosomal membrane in the lysosomal membrane allows the degradation of the remaining inner single membrane and the cytoplasmic content of the autophagosome by lysosomal hydrolases. The molecular machinery and the signaling cascades that regulate autophagy are very complex and beyond the scope of this review, but they are nicely reviewed elsewhere. 3,4 Autophagy generally acts as a housekeeping mechanism, and it is crucially involved in the maintenance of normal cellular homeostasis. When stimulated by cellular stress conditions, autophagy functions as a self-cannibalization pathway that promotes cell survival in an unfavorable environment. Preclinical studies have demonstrated that autophagy is associated with cancer, neurodegenerative disorders (eg, Alzheimer, Parkinson, and Huntington diseases), embryogenesis, aging, and immunity, and also with cardiovascular disease, including ischemia-reperfusion injury of the heart, cardiomyopathy, and atherosclerosis. 5-9 Despite tremendous recent advances in the field, the functional significance of autophagy in human disease remain...

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Oxidized LDLs trigger endoplasmic reticulum stress and autophagy: Prevention by HDLs

Cited by 53 publications

References 0 publications

Autophagy in cardiovascular biology

Autophagy in cardiovascular biology

The Changing Face of HDL and the Best Way to Measure It

Autophagy in Atherosclerosis

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