Angiotensin Converting Enzyme 2 Suppresses Pathological Hypertrophy, Myocardial Fibrosis and Diastolic Dysfunction

Oudit, Gavin Y.; Zhong, Jiuchang; Basu, Ratnadeep; Guo, Danny; Penninger, Josef; Kassiri, Zamaneh

doi:10.1016/j.cardfail.2010.06.054

Cited by 6 publications

(7 citation statements)

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“…It is responsible for converting angiotensin (Ang) I into Ang 1‐9 and Ang II into Ang 1‐7, which act on the MAS‐receptor 16,17 . The ACE2/Ang1‐7, Ang1‐9/MAS axis counterbalances the ACE1/AngII/AT1R axis, enabling protection against fibrosis, pulmonary injury, diabetic cardiovascular complications, myocardial infarction, and disseminated intravascular coagulation (DIC), all of which are associated with severe Covid‐19 outcomes 18‐20 . Therefore, decreased tissue ACE2 might be a Covid‐19 risk factor 21 …”

Section: Ace2/tmprss2/adam17 Interplay and Pathophysiology Of Covid‐19mentioning

confidence: 99%

“…16,17 The ACE2/ Ang1-7, Ang1-9/MAS axis counterbalances the ACE1/AngII/AT1R axis, enabling protection against fibrosis, pulmonary injury, diabetic cardiovascular complications, myocardial infarction, and disseminated intravascular coagulation (DIC), all of which are associated with severe Covid-19 outcomes. [18][19][20] Therefore, decreased tissue ACE2 might be a Covid-19 risk factor. 21 Indeed, ACE2 plasma levels are low in healthy individuals and increase during male ageing process.…”

Section: Ace2/tmprss2/adam17 Interplay and Pathophysiology Of Covid-19mentioning

confidence: 99%

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Alpha‐1‐antitrypsin: A possible host protective factor against Covid‐19

Loyola

Reis

Oliveira

et al. 2020

Reviews in Medical Virology

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Summary Understanding Covid‐19 pathophysiology is crucial for a better understanding of the disease and development of more effective treatments. Alpha‐1‐antitrypsin (A1AT) is a constitutive tissue protector with antiviral and anti‐inflammatory properties. A1AT inhibits SARS‐CoV‐2 infection and two of the most important proteases in the pathophysiology of Covid‐19: the transmembrane serine protease 2 (TMPRSS2) and the disintegrin and metalloproteinase 17 (ADAM17). It also inhibits the activity of inflammatory molecules, such as IL‐8, TNF‐α, and neutrophil elastase (NE). TMPRSS2 is essential for SARS‐CoV‐2‐S protein priming and viral infection. ADAM17 mediates ACE2, IL‐6R, and TNF‐α shedding. ACE2 is the SARS‐CoV‐2 entry receptor and a key component for the balance of the renin‐angiotensin system, inflammation, vascular permeability, and pulmonary homeostasis. In addition, clinical findings indicate that A1AT levels might be important in defining Covid‐19 outcomes, potentially partially explaining associations with air pollution and with diabetes. In this review, we focused on the interplay between A1AT with TMPRSS2, ADAM17 and immune molecules, and the role of A1AT in the pathophysiology of Covid‐19, opening new avenues for investigating effective treatments.

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Section: Ace2/tmprss2/adam17 Interplay and Pathophysiology Of Covid‐19mentioning

confidence: 99%

Section: Ace2/tmprss2/adam17 Interplay and Pathophysiology Of Covid-19mentioning

confidence: 99%

Alpha‐1‐antitrypsin: A possible host protective factor against Covid‐19

Loyola

Reis

Oliveira

et al. 2020

Reviews in Medical Virology

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“…Vitamin D receptors can regulate the ACE2 receptors [117]. ACE2 deficiency is also associated with worsening hypertension and cardiac hypertrophy, which is induced by angiotensin II [118].…”

Section: Vitamin D In Comorbidities Of Covid-19mentioning

confidence: 99%

Rays of immunity: Role of sunshine vitamin in management of COVID-19 infection and associated comorbidities

Kumar

Garapati

Murti

et al. 2021

Clinical Nutrition ESPEN

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The catastrophic pandemic engendered due to the Novel coronavirus (COVID-19) outbreak which causes severe clinical afflictions on the respiratory system has severely high morbidity and mortality rates. The requirement of novel compounds is at utmost importance due to lack of targeted drug molecule to treat the afflictions and restrict the viral infection and for the usage of prophylactic treatment to avoid the spread of the infection is of utmost importance. Vitamin D is one such naturally available multifunctional molecule, which plays an eminent role in the immune system and instigation of numerous cellular pathways further promoting health benefits and enhancing the human quality of life. This article reviews the current standpoint scenario and future prevalence of vitamin D supplementation in the management of covid-19 patients. Novel findings of Vitamin D suggest that along with regulation of cell growth, neuroprotective and mood-stabilizing effects, it regulates the immune response also modulate cytokine Interleukin-6 (IL-6) by inducing progesterone-induced blocking factor (PIBF), given the IL-6 levels are considerably high in COVID-19 patients which increases the further complications. Vitamin D also have its effect on angiotensin converting enzyme (ACEII) inhibitor through which the COVID-19 virus makes cell entry. Numerous research data elucidate the play of Vitamin D, in complications of COVID-19 including the most common comorbid conditions, neurological manifestations and immunological aspects makes it an ideal molecule for adjuvant therapy. Including Vitamin D as add-on therapy in the management of COVID-19 might aid the arrest of infection and helps fight this arduous epidemic.

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“…Ang II is a biologically active hormone. It triggers several signaling pathways, which chronically lead to myocardial hypertrophy and increased fibrosis [ 27 , 28 ] toward heart failure [ 29 ]. Ang II is also the molecule responsible for endothelial dysfunction, hypertension, vascular remodeling, and atherosclerosis [ 30 , 31 ].…”

Section: Ras Systemmentioning

confidence: 99%

Angiotensin-converting enzyme 2: a double-edged sword in COVID-19 patients with an increased risk of heart failure

Razeghian‐Jahromi

Zibaeenezhad

et al. 2020

Heart Fail Rev

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The coronavirus disease (COVID-19) pandemic is a global health priority. Given that cardiovascular diseases (CVD) are the leading cause of morbidity around the world and that several trials have reported severe cardiovascular damage in patients infected with SARS-CoV-2, a substantial number of COVID-19 patients with underlying cardiovascular diseases need to continue their medications in order to improve myocardial contractility and to prevent the onset of major adverse cardiovascular events (MACEs), including heart failure. Some of the current life-saving medications may actually simultaneously expose patients to a higher risk of severe COVID-19. Angiotensinconverting enzyme 2 (ACE2), a key counter regulator of the renin-angiotensin system (RAS), is the main entry gate of SARS-CoV-2 into human host cells and an established drug target to prevent heart failure. In fact, ACE inhibitors, angiotensin II receptor blockers, and mineralocorticoid antagonists may augment ACE2 levels to protect organs from angiotensin II overload. Elevated ACE2 expression on the host cell surface might facilitate viral entrance, at the same time sudden nonadherence to these medications triggers MACEs. Hence, safety issues in the use of RAS inhibitors in COVID-19 patients with cardiac dysfunction remain an unsolved dilemma and need paramount attention. Although ACE2 generally plays an adaptive role in both healthy subjects and patients with systolic and/or diastolic dysfunction, we conducted a literature appraisal on its maladaptive role. Understanding the exact role of ACE2 in COVID-19 patients at risk of heart failure is needed to safely manage RAS inhibitors in frail and non-frail critically ill patients.

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Angiotensin Converting Enzyme 2 Suppresses Pathological Hypertrophy, Myocardial Fibrosis and Diastolic Dysfunction

Cited by 6 publications

References 0 publications

Alpha‐1‐antitrypsin: A possible host protective factor against Covid‐19

Alpha‐1‐antitrypsin: A possible host protective factor against Covid‐19

Rays of immunity: Role of sunshine vitamin in management of COVID-19 infection and associated comorbidities

Angiotensin-converting enzyme 2: a double-edged sword in COVID-19 patients with an increased risk of heart failure

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