MicroRNA‐302c‐3p inhibits endothelial cell pyroptosis via directly targeting NOD‐, LRR‐ and pyrin domain‐containing protein 3 in atherosclerosis

J Cellular Molecular Medi

et al. 2021

Self Cite

As a common air pollutant, formaldehyde is widely present in nature, industrial production and consumer products. Endogenous formaldehyde is mainly produced through the oxidative deamination of methylamine catalysed by semicarbazide‐sensitive amine oxidase (SSAO) and is ubiquitous in human body fluids, tissues and cells. Vascular endothelial cells and smooth muscle cells are rich in this formaldehyde‐producing enzyme and are easily damaged owing to consequent cytotoxicity. Consistent with this, increasing evidence suggests that the cardiovascular system and stages of heart development are also susceptible to the harmful effects of formaldehyde. Exposure to formaldehyde from different sources can induce heart disease such as arrhythmia, myocardial infarction (MI), heart failure (HF) and atherosclerosis (AS). In particular, long‐term exposure to high concentrations of formaldehyde in pregnant women is more likely to affect embryonic development and cause heart malformations than long‐term exposure to low concentrations of formaldehyde. Specifically, the ability of mouse embryos to effect formaldehyde clearance is far lower than that of the rat embryos, more readily allowing its accumulation. Formaldehyde may also exert toxic effects on heart development by inducing oxidative stress and cardiomyocyte apoptosis. This review focuses on the current progress in understanding the influence and underlying mechanisms of formaldehyde on cardiovascular disease and heart development.

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

The cellular function and molecular mechanism of formaldehyde in cardiovascular disease and heart development

Zhang

J Cellular Molecular Medi

et al. 2021

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“…The endothelium plays a pivotal role in the progression of AS and its complications, and endothelial dysfunction is widely recognized as one of the early alterations in the vessel wall preceding the development of plaques [24,25]. Emerging evidence has shown that the degree of endothelial cell (EC) apoptosis may be a key factor in the transition of a plaque from a stable state to a fragile state [26,27]. The glycolytic enzyme 6-phosphofructo-2-kinase/ fructose-2,6-biphosphatase (PFKFB3) is highly expressed in the ECs present in vulnerable human carotid atherosclerotic plaques, and inhibition of PFKFB3 activity reduces cell apoptosis in plaques and promotes plaque stability [28].…”

Section: Endothelial Cellsmentioning

confidence: 99%

Targeting non-coding RNAs in unstable atherosclerotic plaques: Mechanism, regulation, possibilities, and limitations

Wang

et al. 2021

Int. J. Biol. Sci.

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Cardiovascular diseases (CVDs) caused by arteriosclerosis are the leading cause of death and disability worldwide. In the late stages of atherosclerosis, the atherosclerotic plaque gradually expands in the blood vessels, resulting in vascular stenosis. When the unstable plaque ruptures and falls off, it blocks the vessel causing vascular thrombosis, leading to strokes, myocardial infarctions, and a series of other serious diseases that endanger people's lives. Therefore, regulating plaque stability is the main means used to address the high mortality associated with CVDs. The progression of the atherosclerotic plaque is a complex integration of vascular cell apoptosis, lipid metabolism disorders, inflammatory cell infiltration, vascular smooth muscle cell migration, and neovascular infiltration. More recently, emerging evidence has demonstrated that non-coding RNAs (ncRNAs) play a significant role in regulating the pathophysiological process of atherosclerotic plaque formation by affecting the biological functions of the vasculature and its associated cells. The purpose of this paper is to comprehensively review the regulatory mechanisms involved in the susceptibility of atherosclerotic plaque rupture, discuss the limitations of current approaches to treat plaque instability, and highlight the potential clinical value of ncRNAs as novel diagnostic biomarkers and potential therapeutic strategies to improve plaque stability and reduce the risk of major cardiovascular events.

“… 1 , 2 , 3 The disease is characterized by deposition of lipid and other blood components in the intima of the artery, proliferation of smooth muscle cells and increase of collagen fibres, chronic inflammation, plaque formation and hardening of the vascular walls. 3 , 4 , 5 The development of atheromatous plaques leads to serious clinical outcomes. 6 , 7 Once the vulnerable plaques rupture, they induce several clinical conditions, including stroke and myocardial infarction.…”

Section: Introductionmentioning

confidence: 99%

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mentioning

confidence: 99%

Expression profiles and potential roles of transfer RNA‐derived small RNAs in atherosclerosis

J Cellular Molecular Medi

Wang

et al. 2021

Self Cite

Atherosclerosis (AS), one of the most common cardiovascular diseases, is the primary cause of morbidity and mortality in the case of cardiac events, thus posing a great threat to human health worldwide. [1][2][3] The disease is characterized by deposition of lipid and other blood components in the intima of the artery, proliferation of smooth muscle cells and increase of collagen fibres, chronic inflammation, plaque formation and hardening of the vascular walls. [3][4][5] The development of atheromatous plaques leads to serious clinical outcomes. 6,7 Once the vulnerable plaques rupture, they induce several clinical conditions, including stroke and myocardial infarction. 8 To date, arteriography is considered to be the gold standard for the diagnosis of AS. However, given the involvement of an invasive procedure, primary injury is