Smooth muscle NADPH oxidase 4 promotes angiotensin II-induced aortic aneurysm and atherosclerosis by regulating osteopontin

Yu, Wennian; Li, Xiao; Que, Yumei; Li, Siqi; Chen, Lili; Hu, Pengcheng; Xiong, Rui; Seta, Francesca; Chen, Hao; Tong, Xiaoyong

doi:10.1016/j.bbadis.2020.165912

Cited by 18 publications

(15 citation statements)

References 36 publications

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“…Fourth, the concentration of Ang II used in this study (1 μM) was much higher than what has been reported in the body [ 69 ]. Nonetheless, the 1 μM concentration used is consistent with other in vitro experiments both from our group [ 40 , 70 ] and from many other groups [ [71] , [72] , [73] , [74] , [75] , [76] , [77] , [78] ]. There is a reasonable criticism that Ang II may induce desensitization, downregulation, and internalization of its receptors [ [79] , [80] , [81] ].…”

Section: Discussionsupporting

confidence: 90%

Deficiency of peroxisome proliferator-activated receptor α attenuates apoptosis and promotes migration of vascular smooth muscle cells

Duan

Liu

et al. 2021

Biochemistry and Biophysics Reports

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Peroxisome proliferator-activated receptor (PPAR) α is widely expressed in the vasculature and has pleiotropic and lipid-lowering independent effects, but its role in the growth and function of vascular smooth muscle cells (VSMCs) during vascular pathophysiology is still unclear. Herein, VSMC-specific PPARα-deficient mice ( Ppara ΔSMC ) were generated by Cre-LoxP site-specific recombinase technology and VSMCs were isolated from mice aorta. PPARα deficiency attenuated VSMC apoptosis induced by angiotensin (Ang) II and hydrogen peroxide, and increased the migration of Ang II-challenged cells.

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Section: Discussionsupporting

confidence: 90%

Deficiency of peroxisome proliferator-activated receptor α attenuates apoptosis and promotes migration of vascular smooth muscle cells

Duan

Liu

et al. 2021

Biochemistry and Biophysics Reports

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“… 18 VSMCs can secrete multiple cytokines (interleukin‐6, monocyte chemoattractant protein‐1, interleukin‐1β, and tumor necrosis factor‐α) 53 and chemotactic factors to recruit inflammatory cells to the aortic wall. 4 Multiple signaling pathways, including Janus kinase‐signal transducer and activator of transcription, 54 mammalian target of rapamycin, 55 nicotinamide adenine dinucleotide phosphate oxidase 4, 56 nuclear factor kappa B, 57 switch/sucrose nonfermentable–related, matrix‐associated, actin‐dependent regulator of chromatin, subfamily d, member 1, 58 extracellular signal‐regulated kinases 1/2 59 and Rho kinase 60 promote VSMC inflammation and aortic aneurysm progression. By contrast, several signaling pathways, including Rho GTPase activating protein 18, 61 nuclear factor erythroid 2‐related factor 2, 62 cellular communication network factor 3 63 and peroxisome proliferator‐activated receptor‐gamma, 64 attenuate VSMC inflammation and AAA progression.…”

Section: Role Of Vsmcs In Aortic Aneurysmmentioning

confidence: 99%

“…Nicotinamide adenine dinucleotide phosphate oxidases produce ROS in cells. 56 Deletion of the nicotinamide adenine dinucleotide phosphate oxidase subunit, p47phox attenuates angiotensin II–induced AAA in Apoe ‐/‐ mice. 70 Inducible nitric oxide synthase deletion reduces ROS and inhibits CaCl 2 ‐induced AAA.…”

Section: Role Of Vsmcs In Aortic Aneurysmmentioning

confidence: 99%

Vascular Smooth Muscle Cells in Aortic Aneurysm: From Genetics to Mechanisms

Ren

et al. 2021

JAHA

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Aortic aneurysm, including thoracic aortic aneurysm and abdominal aortic aneurysm, is the second most prevalent aortic disease following atherosclerosis, representing the ninth‐leading cause of death globally. Open surgery and endovascular procedures are the major treatments for aortic aneurysm. Typically, thoracic aortic aneurysm has a more robust genetic background than abdominal aortic aneurysm. Abdominal aortic aneurysm shares many features with thoracic aortic aneurysm, including loss of vascular smooth muscle cells (VSMCs), extracellular matrix degradation and inflammation. Although there are limitations to perfectly recapitulating all features of human aortic aneurysm, experimental models provide valuable tools to understand the molecular mechanisms and test novel therapies before human clinical trials. Among the cell types involved in aortic aneurysm development, VSMC dysfunction correlates with loss of aortic wall structural integrity. Here, we discuss the role of VSMCs in aortic aneurysm development. The loss of VSMCs, VSMC phenotypic switching, secretion of inflammatory cytokines, increased matrix metalloproteinase activity, elevated reactive oxygen species, defective autophagy, and increased senescence contribute to aortic aneurysm development. Further studies on aortic aneurysm pathogenesis and elucidation of the underlying signaling pathways are necessary to identify more novel targets for treating this prevalent and clinical impactful disease.

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“…It is hence suggested that ER stress is involved in homocysteine‐induced phenotypic transition of SMCs (Lin et al, 2018; Navas‐Madronal et al, 2019). Our study discovered that OPN could up‐regulate MMP2, Col I, Col III, and VCAM1 in mouse aortic SMCs, which would then promote cell proliferation, migration, and macrophage adhesion (Yu et al, 2020). Importantly, we found that ER stress could up‐regulate the expression of OPN and the up‐regulated OPN could in turn further enhance ER stress.…”

Section: Discussionmentioning

confidence: 95%

Substitution of SERCA2 Cys⁶⁷⁴ accelerates aortic aneurysm by inducing endoplasmic reticulum stress and promoting cell apoptosis

Wang

Yang

Wang

et al. 2022

British J Pharmacology

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Background and Purpose: The Cys 674 residue (C674) in the sarcoplasmic/ endoplasmic reticulum Ca 2+ ATPase 2 (SERCA2) is key to maintaining its enzyme activity. The irreversible oxidation of C674 occurs broadly in aortic aneurysms. Substitution of C674 promotes a phenotypic transition of aortic smooth muscle cells (SMCs) and exacerbates angiotensin II-induced aortic aneurysm. However, its underlying mechanism remains enigmatic.Experimental Approach: Heterozygous SERCA2 C674S knock-in (SKI) mice, in which half of C674 was replaced by serine, were used to mimic partially irreversible oxidation of C674 thiol. The aortas of SKI mice and their littermate wild-type mice under an LDL receptor-deficient background were collected for histological and immunohistochemical analysis. Cultured aortic SMCs were used for protein expression, apoptosis analysis, and cell function studies.

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Smooth muscle NADPH oxidase 4 promotes angiotensin II-induced aortic aneurysm and atherosclerosis by regulating osteopontin

Cited by 18 publications

References 36 publications

Deficiency of peroxisome proliferator-activated receptor α attenuates apoptosis and promotes migration of vascular smooth muscle cells

Deficiency of peroxisome proliferator-activated receptor α attenuates apoptosis and promotes migration of vascular smooth muscle cells

Vascular Smooth Muscle Cells in Aortic Aneurysm: From Genetics to Mechanisms

Substitution of SERCA2 Cys⁶⁷⁴ accelerates aortic aneurysm by inducing endoplasmic reticulum stress and promoting cell apoptosis

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Smooth muscle NADPH oxidase 4 promotes angiotensin II-induced aortic aneurysm and atherosclerosis by regulating osteopontin

Cited by 18 publications

References 36 publications

Deficiency of peroxisome proliferator-activated receptor α attenuates apoptosis and promotes migration of vascular smooth muscle cells

Deficiency of peroxisome proliferator-activated receptor α attenuates apoptosis and promotes migration of vascular smooth muscle cells

Vascular Smooth Muscle Cells in Aortic Aneurysm: From Genetics to Mechanisms

Substitution of SERCA2 Cys674 accelerates aortic aneurysm by inducing endoplasmic reticulum stress and promoting cell apoptosis

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Substitution of SERCA2 Cys⁶⁷⁴ accelerates aortic aneurysm by inducing endoplasmic reticulum stress and promoting cell apoptosis