Alteration of Cardiac ACE2/Mas Expression and Cardiac Remodelling in Rats with Aortic Constriction

Zhang, Yanling; Li, Bing; Wang, Bingxiangi; Zhang, Jingjun; Wu, Junyan; Morgan, Trefor

doi:10.4077/cjp.2014.bad268

Cited by 29 publications

(26 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…2a and b) (Gallagher et al 2008; Zhang et al 2014; Zhu et al 2015). Thus our data show the benefit of ARBs in the treatment of MPS cardiac symptomology and supports our model for cardiac disease and therapeutic effect shown in Fig.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin receptor blockade mediated amelioration of mucopolysaccharidosis type I cardiac and craniofacial pathology

Osborn

Webber

McElmurry

et al. 2016

J of Inher Metab Disea

View full text Add to dashboard Cite

Mucopolysaccharidosis type I (MPS IH) is a lysosomal storage disease (LSD) caused by inactivating mutations to the alpha-L-iduronidase (IDUA) gene. Treatment focuses on IDUA enzyme replacement and currently employed methods can be non-uniform in their efficacy particularly for the cardiac and craniofacial pathology. Therefore, we undertook efforts to better define the pathological cascade accounting for treatment refractory manifestations and demonstrate a role for the renin angiotensin system (RAS) using the IDUA −/− mouse model. Perturbation of the RAS in the aorta was more profound in male animals suggesting a causative role in the observed gender dimorphism and angiotensin receptor blockade (ARB) resulted in improved cardiac function. Further, we show the ability of losartan to prevent shortening of the snout, a common craniofacial anomaly in IDUA −/− mice. These data show a key role for the RAS in MPS associated pathology and support the inclusion of losartan as an augmentation to current therapies.

show abstract

Section: Discussionmentioning

confidence: 99%

Angiotensin receptor blockade mediated amelioration of mucopolysaccharidosis type I cardiac and craniofacial pathology

Osborn

Webber

McElmurry

et al. 2016

J of Inher Metab Disea

View full text Add to dashboard Cite

show abstract

“…29 Myocardial ACE2 protein levels were decreased in pressure-overload-induced HF, suggesting an inverse relationship between myocardial ACE2 protein levels and disease progression. 22, 67 In addition, loss of ACE2 resulted in worsened pathological remodeling in response to pressure-overload-induced biomechanical stress. This was associated with systolic dysfunction and ventricular dilation.…”

Section: Role Of Ace2/ang 1–7 In Hfmentioning

confidence: 99%

“…A779, a MasR antagonist, has been shown to block the majority of Ang 1–7 effects. 17, 19–22 Ang 1–9 has also shown beneficial biological effects via AT 2 R that result in cardioprotection. 23–26 Thus, while ACE/Ang II/AT 1 R is a well-established axis of the RAS, the ACE2/Ang 1–7/MasR and ACE2/Ang 1–9/AT 2 R axes have emerged as physiological antagonists that counter-regulate the activate RAS.…”

mentioning

confidence: 99%

Role of the ACE2/Angiotensin 1–7 Axis of the Renin–Angiotensin System in Heart Failure

Patel

Zhong

Grant

et al. 2016

Circulation Research

739

704

View full text Add to dashboard Cite

Heart failure remains the most common cause of death and disability, and a major economic burden, in industrialized nations. Physiological, pharmacological, and clinical studies have demonstrated that activation of the renin-angiotensin system is a key mediator of heart failure progression. Angiotensin converting enzyme 2 (ACE2), a homologue of ACE, is a monocarboxypeptidase that converts angiotensin II (Ang II) into angiotensin 1–7 (Ang 1–7) which, by virtue of its actions on the Mas receptor, opposes the molecular and cellular effects of Ang II. ACE2 is widely expressed in cardiomyocytes, cardiofibroblasts, and coronary endothelial cells. Recent preclinical translational studies confirmed a critical counter-regulatory role of ACE2/Ang 1–7 axis on the activated renin-angiotensin system that results in heart failure with preserved ejection fraction. While loss of ACE2 enhances susceptibility to heart failure, increasing ACE2 level prevents and reverses the heart failure phenotype. ACE2 and Ang 1–7 have emerged as a key protective pathway against heart failure with reduced and preserved ejection fraction. Recombinant human ACE2 has been tested in phase I and II clinical trials without adverse effects while lowering and increasing plasma Ang II and Ang 1–7 levels, respectively. This review discusses the transcriptional and post-transcriptional regulation of ACE2 and the role of the ACE2/Ang 1–7 axis in cardiac physiology and in the pathophysiology of heart failure. The pharmacological and therapeutic potential of enhancing ACE2/Ang 1–7 action as a novel therapy for heart failure is highlighted.

show abstract

“…The flavonoids quercetin analog forms chelate complex with zinc and inhibit the ACE enzyme (Actis-Goretta et al, 2006; Guerrero et al, 2012). The ACE2 and Mas receptors are involved in the cardiac hypertrophy as their reduced expression is found in hypertrophied heart (Zhang et al, 2014). ACE2, by degradation of Ang II, forms Ang (1–7) which opposes actions of Ang II by binding to the Mas receptor leading to vasodilation, anti-hypertrophic and anti-fibrotic effect (Dias-Peixoto et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Cardioprotective Effect of Ulmus wallichiana Planchon in β-Adrenergic Agonist Induced Cardiac Hypertrophy

et al. 2016

View full text Add to dashboard Cite

Ulmus wallichiana Planchon (Family: Ulmaceae), a traditional medicinal plant, was used in fracture healing in the folk tradition of Uttarakhand, Himalaya, India. The present study investigated the cardioprotective effect of ethanolic extract (EE) and butanolic fraction (BF) of U. wallichiana in isoprenaline (ISO) induced cardiac hypertrophy in Wistar rats. Cardiac hypertrophy was induced by ISO (5 mg/kg/day, subcutaneously) in rats. Treatment was performed by oral administration of EE and BF of U. wallichiana (500 and 50 mg/kg/day). The blood pressure (BP) and heart rate (HR) were measured by non-invasive blood pressure measurement technique. Plasma renin, Ang II, NO, and cGMP level were estimated using an ELISA kit. Angiotensin converting enzyme activity was estimated. BP and HR were significantly increased in ISO group (130.33 ± 1.67 mmHg vs. 111.78 ± 1.62 mmHg, p < 0.001 and 450.51 ± 4.90 beats/min vs. 347.82 ± 6.91 beats/min, respectively, p < 0.001). The BP and HR were significantly reduced (EE: 117.53 ± 2.27 mmHg vs. 130.33 ± 1.67 mmHg, p < 0.001, BF: 119.74 ± 3.32 mmHg vs. 130.33 ± 1.67 mmHg, p < 0.001); HR: (EE: 390.22 ± 8.24 beats/min vs. 450.51 ± 4.90 beats/min, p < 0.001, BF: 345.38 ± 6.79 beats/min vs. 450.51 ± 4.90 beats/min, p < 0.001) after the treatment of EE and BF of U. wallichiana, respectively. Plasma renin, Ang II, ACE activity was decreased and NO, cGMP level were increased. The EE and BF of U. wallichiana down regulated the expression of ANP, BNP, TNF-α, IL-6, MMP9, β1-AR, TGFβ1 and up regulated NOS3, ACE2 and Mas expression level, respectively. Thus, this study demonstrated that U. wallichiana has cardioprotective effect against ISO induced cardiac hypertrophy.

show abstract

Alteration of Cardiac ACE2/Mas Expression and Cardiac Remodelling in Rats with Aortic Constriction

Cited by 29 publications

References 31 publications

Angiotensin receptor blockade mediated amelioration of mucopolysaccharidosis type I cardiac and craniofacial pathology

Angiotensin receptor blockade mediated amelioration of mucopolysaccharidosis type I cardiac and craniofacial pathology

Role of the ACE2/Angiotensin 1–7 Axis of the Renin–Angiotensin System in Heart Failure

Cardioprotective Effect of Ulmus wallichiana Planchon in β-Adrenergic Agonist Induced Cardiac Hypertrophy

Contact Info

Product

Resources

About