Recent Research Advances in Renin-Angiotensin-Aldosterone System Receptors

Azushima, Kengo; Morisawa, Norihiko; Tamura, Kouichi; Nishiyama, Akira

doi:10.1007/s11906-020-1028-6

Cited by 54 publications

(36 citation statements)

References 113 publications

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“…While the cardiovascular outcomes of ACE2 activity and Ang(1-7) production have been described in reasonable detail, it remains uncertain as to the nature of the receptor mediating these effects. Early studies reported that mitochondrial assembly 1 receptors (MasR) mediated the AngII/AT 1 R antagonistic effect of Ang(1-7) including PI3k/Akt activation of nitric oxide synthase and NO production, vasodilation, and anti-fibrosis effects (Azushima et al, 2020). Yet, recent studies showed that Ang(1-7)-mediated AT 2 R activation might contribute to the protective effect via activation of phosphotyrosine phosphatase and suppression of MAPK activity (Azushima et al, 2020).…”

Section: Molecular Pathways Implicated In the Crosstalk Between Cvd Amentioning

confidence: 99%

“…Early studies reported that mitochondrial assembly 1 receptors (MasR) mediated the AngII/AT 1 R antagonistic effect of Ang(1-7) including PI3k/Akt activation of nitric oxide synthase and NO production, vasodilation, and anti-fibrosis effects (Azushima et al, 2020). Yet, recent studies showed that Ang(1-7)-mediated AT 2 R activation might contribute to the protective effect via activation of phosphotyrosine phosphatase and suppression of MAPK activity (Azushima et al, 2020). Moreover, other studies implicated other Mas-related G protein-coupled receptors as mediators of Ang(1-7) effects in the cardiovascular system (Tetzner et al, 2016).…”

Section: Molecular Pathways Implicated In the Crosstalk Between Cvd Amentioning

confidence: 99%

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Molecular Insights Into SARS COV-2 Interaction With Cardiovascular Disease: Role of RAAS and MAPK Signaling

et al. 2020

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In December 2019, reports of viral pneumonia came out of Wuhan city in Hubei province in China. In early 2020, the causative agent was identified as a novel coronavirus (CoV) sharing some sequence similarity with SARS-CoV that caused the severe acute respiratory syndrome outbreak in 2002. The new virus, named SARS-CoV-2, is highly contagious and spread rapidly across the globe causing a pandemic of what became known as coronavirus infectious disease 2019 (COVID-19). Early observations indicated that cardiovascular disease (CVD) patients are at higher risk of progression to severe respiratory manifestations of COVID-19 including acute respiratory distress syndrome. Moreover, further observations demonstrated that SARS-CoV-2 infection can induce de novo cardiac and vascular damage in previously healthy individuals. Here, we offer an overview of the proposed molecular pathways shared by the pathogenesis of CVD and SARS-CoV infections in order to provide a mechanistic framework for the observed interrelation. We examine the crosstalk between the renin-angiotensin-aldosterone system and mitogen activated kinase pathways that potentially links cardiovascular predisposition and/or outcome to SARS-CoV-2 infection. Finally, we summarize the possible effect of currently available drugs with known cardiovascular benefit on these pathways and speculate on their potential utility in mitigating cardiovascular risk and morbidity in COVID-19 patients.

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Section: Molecular Pathways Implicated In the Crosstalk Between Cvd Amentioning

confidence: 99%

Section: Molecular Pathways Implicated In the Crosstalk Between Cvd Amentioning

confidence: 99%

Molecular Insights Into SARS COV-2 Interaction With Cardiovascular Disease: Role of RAAS and MAPK Signaling

et al. 2020

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“…The physiological function of ang ii and aT1r, as well as their role in the pathogenesis of certain diseases are not completely understood. However, compared with aT1r, it is difficult to investigate the functions of AT2R, at least in part due to the relatively low expression levels in cells (23). Previous studies investigating ang ii and its receptors have primarily focused on the ang ii/aT1r axis (24)(25)(26)(27); therefore, the present study investigated the effects of BPa on hepatic damage and the ang ii/aT1r signaling pathway in a rat model of liver i/r injury.…”

Section: Discussionmentioning

confidence: 99%

“…ang ii receptors are present in two forms: aT1r and aT2r (23). The physiological function of ang ii and aT1r, as well as their role in the pathogenesis of certain diseases are not completely understood.…”

Section: Discussionmentioning

confidence: 99%

BPA disrupts 17‑estradiol‑mediated hepatic protection against ischemia/reperfusion injury in rat liver by upregulating the Ang�II/AT1R signaling pathway

Zhang

Shi

et al. 2020

Mol Med Report

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Bisphenol a (BPa), a xenoestrogen commonly used in plastics, may act as an endocrine disruptor, which indicates that BPa might be a public health risk. The present study aimed to investigate the effect of BPa on 17β-estradiol (e2)-mediated protection against liver ischemia/reperfusion (i/r) injury, and to identify the underlying mechanisms using a rat model. a total of 56 male Sprague dawley rats were randomly divided into the following seven groups: i) Sham; ii) i/r; iii) Sham + BPa; iv) i/r + BPa; v) i/r + e2; vi) i/r + e2 + BPa; and vii) i/r + e2 + BPa + losartan [loS; an angiotensin ii (ang ii) type i receptor (aTir) antagonist]. a rat model of hepatic i/r injury was established by inducing hepatic ischemia for 60 min followed by reperfusion for 24 h. When ischemia was induced, rats were treated with vehicle, e2, BPa or loS. after 24 h of reperfusion, blood samples and hepatic tissues were collected for histopathological and biochemical examinations. The results suggested that 4 mg/kg BPA did not significantly alter the liver function, or Ang II and aT1r expression levels in the Sham and i/r groups. However, 4 mg/kg BPa inhibited e2-mediated hepatic protection by enhancing hepatic necrosis, and increasing the release of alanine transaminase, alkaline phosphatase and total bilirubin (P<0.05). Moreover, BPa increased serum and hepatic ang ii levels, as well as aT1r protein expression levels in the e2-treated rat model of liver i/r injury (P<0.05). loS treatment reversed the negative effects of BPa on hepatic necrosis and liver serum marker levels, although it did not reverse BPa-mediated upregulation of serum and hepatic ang ii levels, or hepatic aT1r expression. Therefore, the present study suggested that BPa disrupted e2-mediated hepatic protection following i/R injury, but did not significantly affect healthy or i/r-injured livers; therefore, the mechanism underlying the effects of BPa may be associated with upregulation of the ang ii/aT1r signaling pathway.

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“…RAS is a complex system of biochemical pathways involving various proteins, enzymes, peptides and receptors. RAS regulates homeostasis systemically (Azushima et al, 2020) as well as locally (De Mello & Frohlich, 2011). When discussing RAS we tend to think of vasorestriction (Benjamin, Collier, & Webb, 1988) and dilation of blood vessels (Vanhoutte e al.,1989) and assign negative and positive connotations to them respectively.…”

Section: Background On the Renin-angiotensin System As It Pertains Tomentioning

confidence: 99%

The Human-Covid Tango: Connecting the Dots

Hamdi¹,

Abdaldayem²

2020

Preprint

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As the world grapples with a hot pandemic with various and expanding epicenters, a flurry of medical and scientific activity has gained speed and momentum in a race to halt Covid-19. Due to the urgency of the situation, publication peer review has been speeded up to get information published and turn the gears of research in search for a cure. A hot and controversial topic has been the connection between Covid-19 and the Renin-angiotensin system (RAS). Covid-19, like Sars before it, enters by way of the Angiotensin Converting Enzyme 2 (ACE2). ACE2 is ubiquitously expressed in many tissues in the body serving as the doorway by which the virus can enter and spread causing inflammatory havoc. Demographic evidence coming out of china and other locations make it clear that the elderly and those suffering cardiovascular complications such as hypertension etc are most at risk. The connection to RAS and the demographic nature of the data coming out has led many to advance hypothesis, recommendations and even therapies based on existing RAS inhibitors and other components of the renin-angiotensin system. It is pertinent to review the literature in the context of our understanding of the renin-angiotesnin system to allow better judgements to be made as well as lines of research initiated advancing a quick resolution to Covid-19.

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Recent Research Advances in Renin-Angiotensin-Aldosterone System Receptors

Cited by 54 publications

References 113 publications

Molecular Insights Into SARS COV-2 Interaction With Cardiovascular Disease: Role of RAAS and MAPK Signaling

Molecular Insights Into SARS COV-2 Interaction With Cardiovascular Disease: Role of RAAS and MAPK Signaling

BPA disrupts 17‑estradiol‑mediated hepatic protection against ischemia/reperfusion injury in rat liver by upregulating the Ang�II/AT1R signaling pathway

The Human-Covid Tango: Connecting the Dots

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