El aumento de la expresión del ARNm de la enzima convertidora de angiotensina I homóloga (ECA-2) inducido por atorvastatina se asocia a menor fibrosis e hipertrofia ventricular izquierda en un modelo de cardiomiopatía diabética

Aguilar, Cristian; Ventura, Freddy; Rodríguez-Delfín, Luis

doi:10.1590/s1726-46342011000200013

Cited by 14 publications

(7 citation statements)

References 28 publications

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“…A study by Tikoo et al found that atorvastatin can upregulate ACE2 expression in cardiac tissue when animals were fed high cholesterol diets [ 27 ]. Similar findings were reported by Aguilar et al in a murine model [ 28 ] and Li et al found rosuvastatin upregulated ACE2 expression in murine vascular smooth muscle cells [ 29 ]. Conclusions from these data highlight the beneficial role of statins in mediating attenuation of cardiovascular risk, however, amidst the current COVID-19 pandemic, there is concern about pharmacologic upregulation of the ACE2 receptor, for example with ACE-inhibitor treatment.…”

Section: Recommendationssupporting

confidence: 88%

Managing hyperlipidaemia in patients with COVID-19 and during its pandemic: An expert panel position statement from HEART UK

Iqbal

Adam

et al. 2020

Atherosclerosis

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Background & aims The emergence of the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) which causes Coronavirus Disease 2019 (COVID-19) has resulted in a worldwide pandemic. SARS-CoV-2 is highly contagious and its severity highly variable. The fatality rate is unpredictable but is amplified by several factors including advancing age, atherosclerotic cardiovascular disease, diabetes mellitus, hypertension and obesity. A large proportion of patients with these conditions are treated with lipid lowering medication and questions regarding the safety of continuing lipid-lowering medication in patients infected with COVID-19 have arisen. Some have suggested they may exacerbate their condition. It is important to consider known interactions with lipid-lowering agents and with specific therapies for COVID-19. This statement aims to collate current evidence surrounding the safety of lipid-lowering medications in patients, who have COVID-19. We offer a consensus view based on current knowledge and we rated the strength and level of evidence for these recommendations. Methods Pubmed, Google scholar and Web of Science were searched extensively for articles using search terms: SARS-CoV-2, COVID-19, coronavirus, Lipids, Statin, Fibrates, Ezetimibe, PCSK9 monoclonal antibodies, nicotinic acid, bile acid sequestrate, nutraceuticals, red yeast rice, Omega-3-Fatty acids, Lomitapide, hypercholesterolaemia, dyslipidaemia and Volanesorsen. Results & Conclusions : There is no evidence currently that lipid lowering therapy is unsafe in patients with COVID-19 infection. Lipid-lowering therapy should not be interrupted because of the pandemic or in patients at increased risk of COVID-19 infection. In patients with confirmed COVID-19, care should be taken to avoid drug interactions, between lipid-lowering medications and drugs that may be used to treat COVID-19, especially in patients with abnormalities in liver function tests.

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Section: Recommendationssupporting

confidence: 88%

Managing hyperlipidaemia in patients with COVID-19 and during its pandemic: An expert panel position statement from HEART UK

Iqbal

Adam

et al. 2020

Atherosclerosis

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“…In a diabetic rat model, the addition of fluvastatin (with insulin) improved cardiac ACE2 expression and decreased myocardial fibrosis when compared to rats treated with insulin alone [ 114 ]. Similar findings were reported in a rat model of diabetic cardiomyopathy, where the addition of atorvastatin improved ACE2 expression and normalized ACE/ACE2 ratio compared to control animals who did not receive atorvastatin [ 115 ]. Measurements of ACE2 mRNA expression were increased in rats who received rosuvastatin compared to controls after vascular balloon injury [ 116 ].…”

Section: Medicationssupporting

confidence: 84%

Angiotensin-Converting Enzyme 2 Expression and Severity of SARS-CoV-2 Infection

et al. 2023

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Angiotensin-converting enzyme 2 (ACE2), first discovered in 2000, serves as an important counterregulatory enzyme to the angiotensin II-mediated vasoconstrictive, pro-inflammatory, and pro-fibrotic actions of the renin–angiotensin system (RAS). Conversion of angiotensin II to the peptide angiotensin 1–7 (ANG 1–7) exerts protective vasodilatory, anti-inflammatory, and anti-fibrotic actions through interaction with the MasR receptor. There are many important considerations when noting the role of ACE2 in the pathogenesis and sequelae of COVID-19 infection. ACE2, in the role of COVID-19 infection, was recognized early in 2020 at the beginning of the pandemic as a cell membrane-bound and soluble binding site for the viral spike protein facilitating entering into tissue cells expressing ACE2, such as the lungs, heart, gut, and kidneys. Mechanisms exist that alter the magnitude of circulating and membrane-bound ACE2 (e.g., SARS-CoV-2 infection, viral variants, patient characteristics, chronic disease states, and the degree of cell surface expression of ACE2) and the influence these mechanisms have on the severity of disease and associated complications (e.g., respiratory failure, systemic inflammatory response syndrome, acute myocarditis, acute kidney injury). Several medications alter the ACE2 receptor expression, but whether these medications can influence the course of the disease and improve outcomes is unclear. In this review, we will discuss what is known about the interrelation of SARS-CoV-2, ACE2 and the factors that may contribute to the variability of its expression and potential contributors to the severity of COVID-19 infection.

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“…[23]. Pathological changes including cell apoptosis [24], fibrosis [25] and cardiac hypertrophy [26] are involved in DCM. More importantly, during the development of DCM, in addition to cardiac pump dysfunction due to loss of contractile units, malignant ventricular arrhythmias such as sudden cardiac death (SCD) were considered contributing more to the mortality in diabetic patients [27,28].…”

Section: Discussionmentioning

confidence: 99%

Protein kinase RNA-like endoplasmic reticulum kinase (PERK)/calcineurin signaling is a novel pathway regulating intracellular calcium accumulation which might be involved in ventricular arrhythmias in diabetic cardiomyopathy

Liu

Cai

Zhu

et al. 2014

Cellular Signalling

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El aumento de la expresión del ARNm de la enzima convertidora de angiotensina I homóloga (ECA-2) inducido por atorvastatina se asocia a menor fibrosis e hipertrofia ventricular izquierda en un modelo de cardiomiopatía diabética

Abstract: Our results indicate that atorvastatin, independently of its cholesterol-lowering capacity, lowers the ACE/ACE2 ratio to normal values and attenuates the development of adverse remodeling in the diabetic heart.

Cited by 14 publications

References 28 publications

Managing hyperlipidaemia in patients with COVID-19 and during its pandemic: An expert panel position statement from HEART UK

Managing hyperlipidaemia in patients with COVID-19 and during its pandemic: An expert panel position statement from HEART UK

Angiotensin-Converting Enzyme 2 Expression and Severity of SARS-CoV-2 Infection

Protein kinase RNA-like endoplasmic reticulum kinase (PERK)/calcineurin signaling is a novel pathway regulating intracellular calcium accumulation which might be involved in ventricular arrhythmias in diabetic cardiomyopathy

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