Physical Exercise Is a Potential “Medicine” for Atherosclerosis

Yang, Jian; Cao, Yanxiang; Gao, Rongrong; Mi, Qiongyao; Dai, Qiying; Zhu, Fubao

doi:10.1007/978-981-10-4307-9_15

Cited by 30 publications

(24 citation statements)

References 168 publications

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“…Exercise can significantly reduce the risk of cardiovascular diseases [22]. A study by Yang et al showed that physical exercise acts as a potential medicine for atherosclerosis, and this study summarizes the mechanisms and clinical applications of exercise [23]. e quality of life and prognosis of patients with heart failure can be improved by exercise training, and the American College of Cardiology/ American Heart Association, European Society of Cardiology, and National Institute for Health and Care Excellence (NICE) have recommended exercise-based cardiac rehabilitation as an adjunct for heart failure patients with unlimited exercise [24].…”

Section: Discussionmentioning

confidence: 88%

Exercise Improves Endothelial Function via the lncRNA MALAT1/miR-320a Axis in Obese Children and Adolescents

Zhao

Yin

Cao

et al. 2021

Cardiology Research and Practice

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Background. Endothelial dysfunction commonly occurs in obese children and adolescents, leading to an increased risk of cardiovascular diseases. Exercise has significant protective effects against endothelial dysfunction through regulating some noncoding RNAs. This study aimed to investigate the relationship of long noncoding RNA MALAT1 and microRNA-320a (miR-320a) with the exercise-induced improvement of endothelial dysfunction in obese children and adolescents. Methods. Sixty obese children and adolescents were included in this study, including 40 cases that received 12-week exercise training and 20 cases that received only diet control. The anthropometric and blood indices before and after exercise were recorded and compared, and the endothelial dysfunction was evaluated by examining the levels of markers, including VCAM-1, ICAM-1, and E-selectin, using an ELISA assay. The expression levels of noncoding RNAs were assessed using real-time quantitative PCR, and their correlation with patients’ recorded indices and endothelial dysfunction markers was analyzed. Results. The 12-week exercise training significantly decreased the levels of VCAM-1, ICAM-1, and E-selectin and could inhibit MALAT1 but promote miR-320a expression in obese children and adolescents. The expression of MALAT1 and miR-320a was correlated with the changes in the anthropometric and blood indices of obese children and adolescents, and their correlations with endothelial dysfunction markers were obtained. Conclusion. All the data revealed that exercise has significantly protective effects against endothelial dysfunction and can regulate the expression of the MALAT1/miR-320a axis. MALAT1 and miR-320a were correlated with endothelial dysfunction markers, indicating that the MALAT1/miR-320a axis may be related with the alleviating effects of exercise on endothelial function in obese children and adolescents.

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Section: Discussionmentioning

confidence: 88%

Exercise Improves Endothelial Function via the lncRNA MALAT1/miR-320a Axis in Obese Children and Adolescents

Zhao

Yin

Cao

et al. 2021

Cardiology Research and Practice

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“…These factors together support normal circulatory function and its adaptive response to adverse environmental challenges, disturbance of which can predispose to atherosclerosis (Kim et al, 2013; Lee et al, 2013). Factors leading to atherosclerosis include consumption of high-fat and cholesterol diet (Marir et al, 2013), dyslipidemia (Sanin et al, 2017), diabetes (Lehrke and Marx, 2017), chronic inflammation (Lee et al, 2018), genetic risk (Whayne, and Saha, 2019), lack of exercise (Yang J. et al, 2017), hypertension (Hurtubise et al, 2016), social stress (Meng et al, 2019), smoking and other unhealthy life-styles or environmental factors (Niemann et al, 2017). As shown in a cohort study in Mexico, the coronary risk factors observed were dyslipidemia (100%), hypertension (86%), obesity/overweight (75%), metabolic syndrome (71%), smoking (68%), and diabetes (58%) (Rettori et al, 2014).…”

Section: Atherosclerosis and Cardioprotective Effect Of Otmentioning

confidence: 99%

Therapeutic Potential of Oxytocin in Atherosclerotic Cardiovascular Disease: Mechanisms and Signaling Pathways

Wang

Yang

et al. 2019

Front. Neurosci.

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Coronary artery disease (CAD) is a major cardiovascular disease responsible for high morbidity and mortality worldwide. The major pathophysiological basis of CAD is atherosclerosis in association with varieties of immunometabolic disorders that can suppress oxytocin (OT) receptor (OTR) signaling in the cardiovascular system (CVS). By contrast, OT not only maintains cardiovascular integrity but also has the potential to suppress and even reverse atherosclerotic alterations and CAD. These protective effects of OT are associated with its protection of the heart and blood vessels from immunometabolic injuries and the resultant inflammation and apoptosis through both peripheral and central approaches. As a result, OT can decelerate the progression of atherosclerosis and facilitate the recovery of CVS from these injuries. At the cellular level, the protective effect of OT on CVS involves a broad array of OTR signaling events. These signals mainly belong to the reperfusion injury salvage kinase pathway that is composed of phosphatidylinositol 3-kinase-Akt-endothelial nitric oxide synthase cascades and extracellular signal-regulated protein kinase 1/2. Additionally, AMP-activated protein kinase, Ca 2+ /calmodulin-dependent protein kinase signaling and many others are also implicated in OTR signaling in the CVS protection. These signaling events interact coordinately at many levels to suppress the production of inflammatory cytokines and the activation of apoptotic pathways. A particular target of these signaling events is endoplasmic reticulum (ER) stress and mitochondrial oxidative stress that interact through mitochondria-associated ER membrane. In contrast to these protective effects and machineries, rare but serious cardiovascular disturbances were also reported in labor induction and animal studies including hypotension, reflexive tachycardia, coronary spasm or thrombosis and allergy. Here, we review our current understanding of the protective effect of OT against varieties of atherosclerotic etiologies as well as the approaches and underlying mechanisms of these effects. Moreover, potential cardiovascular disturbances following OT application are also discussed to avoid unwanted effects in clinical trials of OT usages.

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“…These behavioral changes are atheroprotective via metabolic aspects, mutually interconnected. For example, physical activity simultaneously decreases inflammation, oxidative stress, blood pressure, plasma lipids, and increases endothelial function, and muscle energy expenditure [ 127 ]. These cumulative effects are a veritable challenge to compare their benefits with WAT browning.…”

Section: Discussionmentioning

confidence: 99%

Browning of White Adipose Tissue as a Therapeutic Tool in the Fight against Atherosclerosis

2021

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Despite continuous medical advances, atherosclerosis remains the prime cause of mortality worldwide. Emerging findings on brown and beige adipocytes highlighted that these fat cells share the specific ability of non-shivering thermogenesis due to the expression of uncoupling protein 1. Brown fat is established during embryogenesis, and beige cells emerge from white adipose tissue exposed to specific stimuli like cold exposure into a process called browning. The consecutive energy expenditure of both thermogenic adipose tissues has shown therapeutic potential in metabolic disorders like obesity and diabetes. The latest data suggest promising effects on atherosclerosis development as well. Upon cold exposure, mice and humans have a physiological increase in brown adipose tissue activation and browning of white adipocytes is promoted. The use of drugs like β3-adrenergic agonists in murine models induces similar effects. With respect to atheroprotection, thermogenic adipose tissue activation has beneficial outcomes in mice by decreasing plasma triglycerides, total cholesterol and low-density lipoproteins, by increasing high-density lipoproteins, and by inducing secretion of atheroprotective adipokines. Atheroprotective effects involve an unaffected hepatic clearance. Latest clinical data tend to find thinner atherosclerotic lesions in patients with higher brown adipose tissue activity. Strategies for preserving healthy arteries are a major concern for public health.

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Physical Exercise Is a Potential “Medicine” for Atherosclerosis

Cited by 30 publications

References 168 publications

Exercise Improves Endothelial Function via the lncRNA MALAT1/miR-320a Axis in Obese Children and Adolescents

Exercise Improves Endothelial Function via the lncRNA MALAT1/miR-320a Axis in Obese Children and Adolescents

Therapeutic Potential of Oxytocin in Atherosclerotic Cardiovascular Disease: Mechanisms and Signaling Pathways

Browning of White Adipose Tissue as a Therapeutic Tool in the Fight against Atherosclerosis

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