The molecular mechanism of Ang II induced-AAA models based on proteomics analysis in ApoE−/− and CD57BL/6J mice

Ren, Jinrui; Wu, Lianglin; Wu, Jianhuang; Tang, Xiaonan; Lv, Yanze; Wang, Wei; Li, Fangda; Yang, Dan; Liu, Changzheng; Zheng, Yuehong

doi:10.1016/j.jprot.2022.104702

Cited by 5 publications

(6 citation statements)

References 47 publications

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“…Arterial endothelium is the site of key dolipid changes during atherogenesis [7]. But dysfunction of endotheliocytes and even vascular cell death occurs also early in COVID-19, since SARS-CoV-2 is endotheliotropic [8,12,34]. Damage to the endothelium can be caused both by a direct cytopathic effect of the virus, and by the effects of parietal leukocytes involved in the immune response to the virus.…”

Section: Endothelial Dysfunction In Covid-19 and Atherosclerosis: Com...mentioning

confidence: 99%

“…Damage to the endothelium can be caused both by a direct cytopathic effect of the virus, and by the effects of parietal leukocytes involved in the immune response to the virus. Several pathways are involved in the development of endothelial-mediated complications of COVID-19 [8,34,35].…”

Section: Endothelial Dysfunction In Covid-19 and Atherosclerosis: Com...mentioning

confidence: 99%

“…Analysis of differentially expressed genes in cardiomyocytes has shown that this protein is the most important "coupler" of atherogenesis and pathogenesis of COVID-19. Protein MyD88, either by activating the transcription factor NF-κB, or by itself, initiates the expression of pro-inflammatory cytokines and chemokines -CXCL1, CXCL2, CXCL3, CXCL8 and IL-1β, which promotes local inflammation in the myocardium and in the vascular wall, as well as excessive systemic hypercytokinemia, up to its extreme degree -"cytokine storm", sometimes resulting in the hemodynamic shock [1,34].…”

Section: Endothelial Dysfunction In Covid-19 and Atherosclerosis: Com...mentioning

confidence: 99%

“…Ang-II is closely associated with atherosclerosis, e.g. it induces the fomation of abdominal aortic aneurysms (atypical complications of atherosclerosis) in mice with dyslipidaemias [34]. Thus, RAAS dysfunction is a common link in the pathogenesis of COVID-19, atherosclerosis, and their complications.…”

Section: The Role Of Dysfunction Of the Renin-angiotensin-aldosterone...mentioning

confidence: 99%

“…Direct cytopathic effect of the virus on endothelial cells [69] Protease activation, causing a transition from a stable to a pathological atherosclerotic injury and the degradation of the plaque protective fibrous cap. [9,42] Leucocyte recruitment and adhesion to the vascular wall [12] Expression of pro-inflammatory chemokines and cytokines (CXCL1, CXCL2, CXCL3, CXCL8, IL-1β) in the vascular wall resulted from the activation of MyD88-dependent pathways [1,34] VEGLX damage [36] Mitochondrial dysfunction leading to the increased production of reactive oxygen species [33] Endothelial damage caused by neutrophil extracellular traps (NETs) [53] Endothelial damage caused by the components of the activated complement system [52] Vasa vasorum vasculitis and/or thrombosis [63] Interestingly, pharmacological agents commonly used in the treatment of atherosclerosis, such as statins and acetylsalicylic acid, seem to reduce both the incidence of serious complications of COVID-19 and the death rate from this infection. The possible effects of chronic therapy with acetylsalicylic acid have not been fully studied.…”

Section: Mechanismsmentioning

confidence: 99%

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Aterosclerosis, Cardiovascular Disorders And Covid-19: Comorbid Pathogenesis

Makarova¹,

Ryabkova²,

Салухов³

et al. 2022

Preprint

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The article describes how atherosclerosis and coronavirus disease 19 (COVID-19) may affect each other. The features of this comorbid pathogenesis at various levels (vascular, cellular and molecular) are considered. A bidirectional influence of these conditions is described: the presence of cardiovascular diseases affects different individual susceptibility to viral infection. In turn, SARS-CoV-2 can have a negative effect on the endothelium and cardiomyocytes, causing blood clotting, secretion of pro-inflammatory cytokines, and thus exacerbating the development of atherosclerosis. In addition to the established entry into cells via ACE2 принимая во внимание его влияние на, other mechanisms of SARS-CoV-2 entry are currently under investigation, for example, through CD147. Pathogenesis of comorbidity can be determined by the influence of the virus on various links which are meaningful for atherogenesis: generation of oxidized forms of LDL, launch of a cytokine storm, damage to the endothelial glycocalyx, and mitochondrial injury. The transformation of a stable plaque into an unstable one plays an important role in the pathogenesis of atherosclerosis complications and can be triggered by COVID-19. The impact of SARS-CoV-2 on large vessels such as aorta is more complex than previously thought considering its impact on vasa vasorum. Current information on the mutual influence of the medicines used in the treatment of atherosclerosis and acute COVID-19 is briefly summarized

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Section: Endothelial Dysfunction In Covid-19 and Atherosclerosis: Com...mentioning

confidence: 99%

Section: Endothelial Dysfunction In Covid-19 and Atherosclerosis: Com...mentioning

confidence: 99%

Section: Endothelial Dysfunction In Covid-19 and Atherosclerosis: Com...mentioning

confidence: 99%

Section: The Role Of Dysfunction Of the Renin-angiotensin-aldosterone...mentioning

confidence: 99%

Section: Mechanismsmentioning

confidence: 99%

See 3 more Smart Citations

Aterosclerosis, Cardiovascular Disorders And Covid-19: Comorbid Pathogenesis

Makarova¹,

Ryabkova²,

Салухов³

et al. 2022

Preprint

View full text Add to dashboard Cite

show abstract

Orosomucoid 2 as a biomarker of carotid artery atherosclerosis plaque vulnerability through its generation of reactive oxygen species and lipid accumulation in vascular smooth muscle cells

Che,

Ren,

Zhao

et al. 2024

Biochemical and Biophysical Research Communications

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Novel formylpeptide receptor 1/2 agonist limits hypertension-induced cardiovascular damage

Singh,

Jackson,

Fang

et al. 2024

Cardiovascular Research

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Aims Formylpeptide receptors (FPRs) play a critical role in the regulation of inflammation, an important driver of hypertension-induced end-organ damage. We have previously reported that the biased FPR small-molecule agonist, compound17b (Cmpd17b), is cardioprotective against acute, severe inflammatory insults. Here, we reveal the first compelling evidence of the therapeutic potential of this novel FPR agonist against a longer-term, sustained inflammatory insult, i.e. hypertension-induced end-organ damage. The parallels between the murine and human hypertensive proteome were also investigated. Methods and results The hypertensive response to angiotensin II (Ang II, 0.7 mg/kg/day, s.c.) was attenuated by Cmpd17b (50 mg/kg/day, i.p.). Impairments in cardiac and vascular function assessed via echocardiography were improved by Cmpd17b in hypertensive mice. This functional improvement was accompanied by reduced cardiac and aortic fibrosis and vascular calcification. Cmpd17b also attenuated Ang II-induced increased cardiac mitochondrial complex 2 respiration. Proteomic profiling of cardiac and aortic tissues and cells, using label-free nano-liquid chromatography with high-sensitivity mass spectrometry, detected and quantified ∼6000 proteins. We report hypertension-impacted protein clusters associated with dysregulation of inflammatory, mitochondrial, and calcium responses, as well as modified networks associated with cardiovascular remodelling, contractility, and structural/cytoskeletal organization. Cmpd17b attenuated hypertension-induced dysregulation of multiple proteins in mice, and of these, ∼110 proteins were identified as similarly dysregulated in humans suffering from adverse aortic remodelling and cardiac hypertrophy. Conclusion We have demonstrated, for the first time, that the FPR agonist Cmpd17b powerfully limits hypertension-induced end-organ damage, consistent with proteome networks, supporting development of pro-resolution FPR-based therapeutics for treatment of systemic hypertension complications.

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The molecular mechanism of Ang II induced-AAA models based on proteomics analysis in ApoE−/− and CD57BL/6J mice

Cited by 5 publications

References 47 publications

Aterosclerosis, Cardiovascular Disorders And Covid-19: Comorbid Pathogenesis

Aterosclerosis, Cardiovascular Disorders And Covid-19: Comorbid Pathogenesis

Orosomucoid 2 as a biomarker of carotid artery atherosclerosis plaque vulnerability through its generation of reactive oxygen species and lipid accumulation in vascular smooth muscle cells

Novel formylpeptide receptor 1/2 agonist limits hypertension-induced cardiovascular damage

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