Swimming exercise activates aortic autophagy and limits atherosclerosis in ApoE−/− mice

Li, Yang; Sun, Dakang; Zheng, Yuanyuan; Cheng, Yiyun

doi:10.1016/j.orcp.2020.04.008

Cited by 11 publications

(11 citation statements)

References 36 publications

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“…[14][15][16] A recent study has documented that forced long-term swimming exercise reduces circulating lipid levels, increases autophagy protein expression and reduces atherosclerotic plaque formation in the aorta of ApoE mice on a western diet. 31 However, whether the increases in autophagy protein were secondary to an improvement in the circulating lipid profile of ApoE mice remained to be determined. In the present study, we examined if endothelial autophagy is enhanced by 16 weeks of voluntary running, an exercise model that inhibits atherosclerosis in ApoE deficient mice without altering circulating lipids.…”

Section: Discussionmentioning

confidence: 99%

“…Previous reports have documented that regular exercise activates autophagy in skeletal muscle and adipose tissues 14‐16 . A recent study has documented that forced long‐term swimming exercise reduces circulating lipid levels, increases autophagy protein expression and reduces atherosclerotic plaque formation in the aorta of ApoE mice on a western diet 31 . However, whether the increases in autophagy protein were secondary to an improvement in the circulating lipid profile of ApoE mice remained to be determined.…”

Section: Discussionmentioning

confidence: 99%

“…Disruption of endothelial cell homeostasis has been recognized as a hallmark for the development of atherosclerosis. Regular exercise preserves homeostasis in arterial endothelial cells protecting arteries from atherosclerosis likely via multiple mechanisms such as increased blood flow, decreased circulating lipids, as well as reduced obesity and low‐grade inflammation 4,7,29‐31 . From a cellular perspective, however, endothelial cells can become pro‐atherosclerotic and the processes involved are poorly understood.…”

Section: Discussionmentioning

confidence: 99%

“…Regular exercise preserves homeostasis in arterial endothelial cells protecting arteries from atherosclerosis likely via multiple mechanisms such as increased blood flow, decreased circulating lipids, as well as reduced obesity and low-grade inflammation. 4,7,[29][30][31] From a cellular perspective, however, endothelial cells can become proatherosclerotic and the processes involved are poorly understood. In that sense, autophagy plays an important role in the maintenance of endothelial cell homeostasis and it The results also demonstrate a link between enhanced autophagy in endothelial cells and regular exercise-mediated improvement of IL-1 signaling.…”

Section: Discussionmentioning

confidence: 99%

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Regular exercise stimulates endothelium autophagy via IL‐1 signaling in ApoE deficient mice

et al. 2021

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Regular exercise maintains arterial endothelial cell homeostasis and protects the arteries from vascular disease, such as peripheral artery disease and atherosclerosis. Autophagy, which is a cellular process that degrades misfolded or aggregate proteins and damaged organelles, plays an important role in maintaining organ and cellular homeostasis. However, it is unknown whether regular exercise stimulates autophagy in aorta endothelial cells of mice prone to atherosclerosis independently of their circulating lipid profile. Here, we observed that 16 weeks of voluntary exercise reduced high‐fat diet‐induced atherosclerotic plaque formation in the aortic root of ApoE deficient mice, and that this protection occurred without changes in circulating triglycerides, total cholesterol, and lipoproteins. Immunofluorescence analysis indicated that voluntary exercise increased levels of the autophagy protein LC3 in aortic endothelial cells. Interestingly, human umbilical vein endothelial cells (HUVECs) exposed to serum from voluntarily exercised mice displayed significantly increased LC3‐I and LC3‐II protein levels. Analysis of circulating cytokines demonstrated that voluntary exercise caused changes directly relevant to IL‐1 signaling (ie, decreased interleukin‐1 receptor antagonist [IL‐1ra] while also increasing IL‐1α). HUVECs exposed to IL‐1α and IL‐1β recombinant protein significantly increased LC3 mRNA expression, LC3‐I and LC3‐II protein levels, and autophagy flux. Collectively, these results suggest that regular exercise protects arteries from ApoE deficient mice against atherosclerosis at least in part by stimulating endothelial cell autophagy via enhanced IL‐1 signaling.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Regular exercise stimulates endothelium autophagy via IL‐1 signaling in ApoE deficient mice

et al. 2021

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“…A number of studies have also demonstrated that the type, exposure time and magnitude of shear stress affects ICAM-1 expression ( 38-40 ). Acute exercise may increase cardiac ICAM-1 expression accompanied by a significant increase in inflammatory mediators ( 41 ). Melatonin administration reverses this effect, suggesting its protective effect against cardiac damage induced by exercise ( 42 ).…”

Section: Discussionmentioning

confidence: 99%

Melatonin attenuates low shear stress‑induced pyroptosis and endothelial cell dysfunction via the RORα/miR‑223/STAT‑3 signalling pathway

Sui

Yang

2021

Exp Ther Med

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Endothelial cells sense changes in blood flow shear stress and affect the progression of atherosclerotic plaques. Pyroptosis is an inflammatory form of cell death and has been implicated in cardiovascular diseases. Melatonin and its nuclear receptor retinoid-related orphan receptor α (RORα) have protective effects on the development of atherosclerosis. To date, whether melatonin can prevent endothelial cell pyroptosis and dysfunction in pathological shear stress remains unclear. In the present study, human umbilical vein endothelial cells (ECs) were cultured under low shear stress conditions (5 dyne/cm 2 ) for 24 h and treated with or without melatonin (2 µmol/l). The binding sites of the microRNA (miR)-223 promoter and RORα were predicted using the JASPAR website. Expression of pyroptosis-related proteins, including cleaved N-terminal gasdermin D, caspase-1, intercellular adhesion molecule 1 (ICAM-1) and nitric oxide (NO) were assessed. The results indicated that low shear stress increased pyroptosis and ICAM-1 expression, whereas it decreased NO levels. Melatonin alleviated pyroptosis and ICAM-1 expression and increased the production of NO in ECs. Further assessment revealed that low-level shear stress decreased RORα protein and mRNA expression, whereas melatonin would bind to RORα and thereby promoted miR-223 transcription in ECs. The present study also identified signal transducer and activator of transcription 3 (STAT-3) as a potential target gene of miR-223-3p. When transfected with miR-223 inhibitor, ECs up-regulated the expression of pyroptosis-related proteins and ICAM-1, and down-regulated NO levels. By contrast, silencing STAT-3 expression diminished the protective effect of miR-223. These results indicated that melatonin prevented ECs from undergoing pyroptosis and alleviated dysfunction via the RORα/miR-223/STAT-3 signalling pathway. This information could aid in the development of novel therapeutic approaches and provide new insights into atherosclerosis.

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Curcumin Equipped Nanozyme‐Like Metal−Organic Framework Platform for the Targeted Atherosclerosis Treatment with Lipid Regulation and Enhanced Magnetic Resonance Imaging Capability

Lv,

Fang,

Huang

et al. 2024

Advanced Science

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Atherosclerotic cardiovascular disease (ASCVD) has become the leading cause of death worldwide, and early diagnosis and treatment of atherosclerosis (AS) are crucial for reducing the occurrence of acute cardiovascular events. However, early diagnosis of AS is challenging, and oral anti‐AS drugs suffer from limitations like imprecise targeting and low bioavailability. To overcome the aforementioned shortcomings, Cur/MOF@DS is developed, a nanoplatform integrating diagnosis and treatment by loading curcumin (Cur) into metal−organic frameworks with nanozymes and magnetic resonance imaging (MRI) properties. In addition, the surface‐modification of dextran sulfate (DS) enables PCN‐222(Mn) effectively target scavenger receptor class A in macrophages or foam cells within the plaque region. This nanoplatform employs mechanisms that effectively scavenge excessive reactive oxygen species in the plaque microenvironment, promote macrophage autophagy and regulate macrophage polarization to realize lipid regulation. In vivo and in vitro experiments confirm that this nanoplatform has outstanding MRI performance and anti‐AS effects, which may provide a new option for early diagnosis and treatment of AS.

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Swimming exercise activates aortic autophagy and limits atherosclerosis in ApoE−/− mice

Cited by 11 publications

References 36 publications

Regular exercise stimulates endothelium autophagy via IL‐1 signaling in ApoE deficient mice

Regular exercise stimulates endothelium autophagy via IL‐1 signaling in ApoE deficient mice

Melatonin attenuates low shear stress‑induced pyroptosis and endothelial cell dysfunction via the RORα/miR‑223/STAT‑3 signalling pathway

Curcumin Equipped Nanozyme‐Like Metal−Organic Framework Platform for the Targeted Atherosclerosis Treatment with Lipid Regulation and Enhanced Magnetic Resonance Imaging Capability

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