Involvement of Angiotensin II Type 1 and 2 Receptors in Gelatinase Regulation in Human Carotid Atheroma &lt;i&gt;in vitro &lt;/i&gt;

Clancy, Paula; Koblar, Simon; Golledge, Jonathan

doi:10.5551/jat.31401

Cited by 6 publications

(4 citation statements)

References 50 publications

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“…However, our data at least indicated that ANG II‐AT 1 R axis played important roles in EAM development and CD11b + Ly6C + cells reprogramming. And our data also were in line with published reports that most actions of ANG II were primarily carried out by AT 1 R signaling . Additionally, inhibition of Erk1/2, p38, or Stat3 could also obviously ameliorate the cardiac injury, which cannot completely owe to prevent M1 polarization; as all these inhibitors are not specific for macrophage polarization, more and more data indicated that macrophage polarization was associated with Erk1/2, p38, or Stat3; therefore, our data suggested that to prevent the macrophage polarization, the EAM development could be ameliorated.…”

Section: Discussionsupporting

confidence: 91%

“…ANG II plays pivotal physiological or pathological roles through ligation with its specific G protein‐coupled receptors, type 1/2 receptor (AT 1 R or AT 2 R). However, most roles were carried out by AT 1 R signaling . Recently, ANG II can serve as a powerful proinflammatory mediator and involve in autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus, autoimmune nephritis, and experimental autoimmune encephalomyelitis as well as monocyte and macrophage recruitment .…”

Section: Introductionmentioning

confidence: 99%

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ANG II facilitated CD11+Ly6Chi cells reprogramming into M1-like macrophage through Erk1/2 or p38-Stat3 pathway and involved in EAM

Shao

et al. 2018

Journal of Leukocyte Biology

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Macrophage, a highly plastic population, is widely distributed. Macrophage functions are settled and acquired polarization programs in response to microenvironmental signals and involved in many inflammatory disorders, such as experimental autoimmune myocarditis (EAM). Phenotypic and functional changes in macrophage are considered as an important determinant of disease progression and/or regression. Angiotensin II (ANG II), as a powerful proinflammatory factor, plays critical roles in inflammatory diseases and macrophage recruitment. It remains unclear whether ANG II contributed to the functional skewing of cardiac infiltrated monocytes/macrophage and involved in EAM development. Therefore, the present work was to address the above questions. Our data showed that ANG II contributed to CD11b Ly6C (CD11b Ly6G Ly6C ) cells reprogramming into M1-like macrophage through Erk1/2 or p38/Stat3 pathway and the reprogramming M1-like cells promoted Th17 cells expansion; abrogation of ANG II-AT R axis significantly ameliorated cardiac injury. The present work first demonstrated a novel immune regulation role of ANG II; ANG II, as a powerful immune factor, promoted CD11b Ly6C inflammatory cells reprogramming into M1-like macrophage and involved in inflammatory disorders development; our results also indicated that ANG II may be a potential therapeutic target for inflammatory diseases.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

ANG II facilitated CD11+Ly6Chi cells reprogramming into M1-like macrophage through Erk1/2 or p38-Stat3 pathway and involved in EAM

Shao

et al. 2018

Journal of Leukocyte Biology

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“…Additionally, inflammatory cells (neutrophils, B- and T-lymphocytes), MMPs and proinflammatory cytokines will be assessed by immunohistochemistry and ELISA as previously described [40, 41]. Circulating concentrations of other AAA biomarkers, including osteoprotegerin, resistin, D-dimer and fasting lipids, will be assessed by ELISA and automated assays as previously described [31, 36–38].…”

Section: Methodsmentioning

confidence: 99%

Fenofibrate in the management of AbdoMinal aortic anEurysm (FAME): study protocol for a randomised controlled trial

Rowbotham

Cavaye

Jaeggi

et al. 2017

Trials

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110

161

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BackgroundAbdominal aortic aneurysm (AAA) is a slowly progressive destructive process of the main abdominal artery. Experimental studies indicate that fibrates exert beneficial effects on AAAs by mechanisms involving both serum lipid modification and favourable changes to the AAA wall.Methods/designFenofibrate in the management of AbdoMinal aortic anEurysm (FAME) is a multicentre, randomised, double-blind, placebo-controlled clinical trial to assess the effect of orally administered therapy with fenofibrate on key pathological markers of AAA in patients undergoing open AAA repair. A total of 42 participants scheduled for an elective open AAA repair will be randomly assigned to either 145 mg of fenofibrate per day or identical placebo for a minimum period of 2 weeks prior to surgery. Primary outcome measures will be macrophage number and osteopontin (OPN) concentration within the AAA wall as well as serum concentrations of OPN. Secondary outcome measures will include levels of matrix metalloproteinases and proinflammatory cytokines within the AAA wall, periaortic fat and intramural thrombus and circulating concentrations of AAA biomarkers.DiscussionAt present, there is no recognised medical therapy to limit AAA progression. The FAME trial aims to assess the ability of fenofibrate to alter tissue markers of AAA pathology.Trial registrationAustralian New Zealand Clinical Trials Registry, ACTRN12612001226897. Registered on 20 November 2012.Electronic supplementary materialThe online version of this article (doi:10.1186/s13063-016-1752-z) contains supplementary material, which is available to authorized users.

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“…In the past decades, the concept of the “vulnerable plaque” has been dominant in the pathogenesis, diagnosis and treatment of ACS, and autopsy studies consistently found that plaques of this morphology were responsible for the majority of fatal myocardial infarcts. A large number of studies indicated that rupture of TCFA is related to the increased breakdown and decreased synthesis of interstitial collagen that forms the fibrous cap [ 10 ]. Interstitial collagen produced by vascular smooth muscle cells (VSMCs) provides strength to the fibrous cap of the plaque.…”

Section: Plaque Rupturementioning

confidence: 99%

New Concepts on the Pathophysiology of Acute Coronary Syndrome

Yuan¹,

Chu²,

Qian³

et al. 2023

Rev. Cardiovasc. Med.

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Acute coronary syndrome (ACS) is the most severe form of ischemic heart disease. Although it is caused by atherosclerotic plaque thrombosis or nonatherosclerotic causes, its pathophysiological mechanism of ACS is not fully understood, and its concept is constantly updated and developed. At present, the main pathophysiological mechanisms include plaque rupture, plaque erosion, calcified nodules (CN) and non-atherosclerotic causes such as coronary vasospasm and myocardial bridging (MB). These mechanisms may overlap and coexist in some ACS patients. Therefore, the pathophysiological mechanism of ACS is complex, and is of great significance for the diagnosis and treatment of ACS. This review will discuss the pathophysiological mechanisms of ACS to provide new thoughts on the pathogenesis, diagnosis and treatment of ACS.

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Involvement of Angiotensin II Type 1 and 2 Receptors in Gelatinase Regulation in Human Carotid Atheroma <i>in vitro </i>

Cited by 6 publications

References 50 publications

ANG II facilitated CD11+Ly6Chi cells reprogramming into M1-like macrophage through Erk1/2 or p38-Stat3 pathway and involved in EAM

ANG II facilitated CD11+Ly6Chi cells reprogramming into M1-like macrophage through Erk1/2 or p38-Stat3 pathway and involved in EAM

Fenofibrate in the management of AbdoMinal aortic anEurysm (FAME): study protocol for a randomised controlled trial

New Concepts on the Pathophysiology of Acute Coronary Syndrome

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