Autophagy in vascular endothelial cells

Jiang, Fan

doi:10.1111/1440-1681.12649

Cited by 108 publications

(87 citation statements)

References 72 publications

(244 reference statements)

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“…Indeed, a careful analysis of existing RTC and related meta-analysis studies on the effects of vitamin D supplementation reveals several methodological limitations, including the use of diverse study populations, different doses of vitamin D with or without Ca 2+ , different durations of supplementation and follow-up, different baseline and acquired circulating 25(OH)D concentrations, and different study outcome parameters [99,201]. Furthermore, significant discrepancies could result from the large inter-individual variation in genetic determinants of the efficacy of vitamin D supplementation [12,109,110], as well as its context-dependent effects on mechanisms in endothelial cells, including autophagy [202]. Consistent with these potential shortcomings in evaluating the effects of vitamin D supplementation, there remains much controversy and an open debate about the reliability of either RCTs or their meta-analyses [99,203,204].…”

Section: Discussionmentioning

confidence: 99%

Vitamin D Deficiency and the Risk of Cerebrovascular Disease

Kim

Perrelli

Ragni³

et al. 2020

Antioxidants

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Vitamin D deficiency has been clearly linked to major chronic diseases associated with oxidative stress, inflammation, and aging, including cardiovascular and neurodegenerative diseases, diabetes, and cancer. In particular, the cardiovascular system appears to be highly sensitive to vitamin D deficiency, as this may result in endothelial dysfunction and vascular defects via multiple mechanisms. Accordingly, recent research developments have led to the proposal that pharmacological interventions targeting either vitamin D deficiency or its key downstream effects, including defective autophagy and abnormal pro-oxidant and pro-inflammatory responses, may be able to limit the onset and severity of major cerebrovascular diseases, such as stroke and cerebrovascular malformations. Here we review the available evidence supporting the role of vitamin D in preventing or limiting the development of these cerebrovascular diseases, which are leading causes of disability and death all over the world.

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Section: Discussionmentioning

confidence: 99%

Vitamin D Deficiency and the Risk of Cerebrovascular Disease

Kim

Perrelli

Ragni³

et al. 2020

Antioxidants

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“…According to the current prediction analysis and luciferase activity determination, ATG16L1 is a target gene of let-7d, and let-7d can negatively regulate ATG16L1. It has previously been reported that various biological factors and chemical compounds are engaged in autophagy in vascular endothelial cells (VEcs), and autophagy has potential effects on endothelial cells (34). There is evidence showing the involvement of miRNAs in autophagy through the regulation of ATGs or their regulators in human diseases (35).…”

Section: Discussionmentioning

confidence: 99%

Emerging roles of let‑7d in attenuating pulmonary arterial hypertension via suppression of pulmonary artery endothelial cell autophagy and endothelin synthesis through ATG16L1 downregulation

Cui

et al. 2020

Int J Mol Med

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Pulmonary arterial hypertension (PAH) is a severe disease characterized by elevated pulmonary arterial pressure and pulmonary vascular resistance, resulting in right ventricular failure and death. compelling evidence has suggested the roles of microRNAs (miRNAs/miRs) in PAH. The present study investigated the possible effects of miR-let-7d on PAH through autophagy-related 16-like 1 (ATG16L1). Initially, the serum levels of let-7d in PAH patients were detected. Rats were then treated with monocrotaline to induce a rat model of PAH, after which the right ventricular systolic pressure (RVSP) and right ventricular hypertrophy index (RVHI) were determined. Next, the putative binding sites between let-7d and ATG16L1 were detected. The expression of let-7d and ATG16L1 in PAH rat models and cells was upregulated or downregulated to assess the effects of these molecules on autophagy in pulmonary artery vascular endothelial cells (PAEcs) and on endothelin synthesis. In addition, the levels of p62, Lc3-I, Lc3-II, Lc3B and endothelin-1 (ET-1) were assessed. The results obtained revealed that let-7d was downregulated in the serum of PAH patients and rats with PAH. Importantly, ATG16L1 was found to be a target gene of let-7d and let-7d could suppress the expression of ATG16L1. Overexpression of let-7d was found to reduce RVSP and RVHI values. Additionally, upregulation of let-7d or depletion of ATG16L1 led to suppression of PAEc autophagy and endothelin synthesis, corresponding to decreased ratios of Lc3-II to Lc3-I and reduced levels of Lc3B but elevated levels of p62 in PAEcs and ET-1 in plasma and lung tissues. In summary, let-7d upregulation alleviates PAH by inhibiting autophagy in PAEcs and suppressing endothelin synthesis through negative regulation of ATG16L1.

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“…Autophagy is widely involved in physiological and pathological activities of endothelial cells. 11 It is worth noting that it can be induced by mechanical and biochemical factors, including shear stress, calcium and oxidative stress, [15][16][17] which are also influenced by decompression-induced intravascular bubbles. [18][19][20][21][22] We speculated that autophagy was probably involved in bubble-induced endothelial injury.…”

Section: Discussionmentioning

confidence: 99%

“…Autophagy, a cellular lysosome‐dependent degradation process, widely participates in physiological and pathological activities of endothelial cells such as proliferation, migration and angiogenesis . The role of autophagy involved in endothelial injury in atherosclerosis, ischaemia‐reperfusion, hepatopulmonary syndrome and other diseases has been well studied .…”

Section: Introductionmentioning

confidence: 99%

Biphasic effects of autophagy on decompression bubble‐induced endothelial injury

Wang¹,

Zhang²,

Nie³

et al. 2019

J Cellular Molecular Medi

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Endothelial dysfunction induced by bubbles plays an important role in decompression sickness (DCS), but the mechanism of which has not been clear. The present study was to investigate the role of autophagy in bubble‐induced endothelial injury. Human umbilical vein endothelial cells (HUVECs) were treated with bubbles, autophagy markers and endothelial injury indices were determined, and relationship strengths were quantified. Effects of autophagy inhibitor 3‐methyladenine (3‐MA) were observed. Bubble contact for 1, 5, 10, 20 or 30 minutes induced significant autophagy with increases in LC3‐II/I ratio and Beclin‐1, and a decrease in P62, which correlated with bubble contact duration. Apoptosis rate, cytochrome C and cleaved caspase‐3 increased, and cell viability decreased following bubble contact for 10, 20 or 30 minutes, but not for 1 or 5 minutes. Injuries in HUVECs were correlated with LC3‐II/I ratio and partially reversed by 3‐MA in 10, 20 or 30 minutes contact, but worsened in 1 or 5 minutes. Bubble pre‐conditioning for 1 minutes resulted in increased cell viability and decreased apoptosis rate compared with no pre‐conditioning, and 30‐minutes pre‐conditioning induced opposing changes, all of which were inhibited by 3‐MA. In conclusion, autophagy was involved and played a biphasic role in bubble‐induced endothelial injury.

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Autophagy in vascular endothelial cells

Abstract: SummaryThe importance of autophagy in cardiovascular physiology and cardiovascular disease is increasingly recognized; however, the precise biological effects and underlying mechanisms of autophagy in the cardiovascular system are still poorly understood. In

Cited by 108 publications

References 72 publications

Vitamin D Deficiency and the Risk of Cerebrovascular Disease

Vitamin D Deficiency and the Risk of Cerebrovascular Disease

Emerging roles of let‑7d in attenuating pulmonary arterial hypertension via suppression of pulmonary artery endothelial cell autophagy and endothelin synthesis through ATG16L1 downregulation

Biphasic effects of autophagy on decompression bubble‐induced endothelial injury

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