Role Of Angiotensin-converting Enzyme Research Articles

Angiotensin-converting enzyme 2: a key enzyme in key organs.

2020 marked the 20th anniversary of the discovery of the angiotensin-converting enzyme 2 (ACE2). This major event that changed the way we see the renin-angiotensin system today could have passed quietly. Instead, the discovery that ACE2 is a major player in the severe acute respiratory syndrome coronavirus 2 pandemic has blown up the literature regarding this enzyme. ACE2 connects the classical arm renin-angiotensin system, consisting mainly of angiotensin II peptide and its AT1 receptor, with a protective arm, consisting mainly of the angiotensin 1-7 peptide and its Mas receptor. In this brief article, we have reviewed the literature to describe how ACE2 is a key protective arm enzyme in the function of many organs, particularly in the context of brain and cardiovascular function, as well as in renal, pulmonary and digestive homeostasis. We also very briefly review and refer to recent literature to present an insight into the role of ACE2 in determining the course of coronavirus diseases 2019.

Vitamin D and COVID-19: Role of ACE2, age, gender, and ethnicity.

Coronavirus disease 2019 (COVID‐19), caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) virus, disproportionally targets older people, particularly men, ethnic minorities, and individuals with underlying diseases such as compromised immune system, cardiovascular disease, and diabetes. The discrepancy in COVID‐19 incidence and severity is multifaceted and likely involves biological, social, as well as nutritional status. Vitamin D deficiency, notably common in Black and Brown people and elderly, is associated with an increased susceptibility to many of the diseases comorbid with COVID‐19. Vitamin D deficiency can cause over‐activation of the pulmonary renin‐angiotensin system (RAS) leading to the respiratory syndrome. RAS is regulated in part at least by angiotensin‐converting enzyme 2 (ACE2), which also acts as a primary receptor for SARS‐CoV‐2 entry into the cells. Hence, vitamin D deficiency can exacerbate COVID‐19, via its effects on ACE2. In this review we focus on influence of age, gender, and ethnicity on vitamin D‐ACE2 interaction and susceptibility to COVID‐19.

Low plasma angiotensin-converting enzyme 2 level in diabetics increases the risk of severe COVID-19 infection.

Patients with pre-existing chronic diseases are more susceptible to coronavirus disease 2019 (COVID-19), yet the underlying causes of increased risk are of infection remain unclear. Angiotensin-converting- enzyme 2 (ACE2), the cell surface receptor that recognizes the coronavirus spike protein has protective effects against inflammation and chronic hyperglycemia in animal models. The roles of ACE2 in severe SARS-CoV-2 infections remains ambiguous due to contradictory findings. In this study, we aimed to investigate the relationship between human plasma ACE2 levels in diabetics and the high risk of severe SARS-CoV-2 infection. First, the medical records of 245 patients with SARS-CoV-2-positive who have chronic diseases were analyzed. We also recruited 404 elderly subjects with comorbid chronic diseases such as diabetes mellitus, coronary heart disease, cerebrovascular disease, hypertension and obesity, and investigated the ACE2 plasma levels. Plasma concentrations of ACE2 were much lower (2973.83±2196.79 pg/mL) in diabetics with chronic disease than in healthy controls (4308.21±2352.42 pg/ml), and the use of hypoglycemia drugs was associated with lower circulating concentrations of ACE2 (P=1.49E-08). Diabetics with lower plasma levels of ACE2 may be susceptible to severe COVID-19. Our findings suggest that the poor prognosis in patients with diabetes infected with SARS-CoV-2 may be due to low circulating ACE2 levels.

The Mechanisms and Animal Models of SARS-CoV-2 Infection.

Coronavirus disease 2019 (COVID-19) is a highly contagious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which has aroused great public health concern worldwide. Currently, COVID-19 epidemic is spreading in many countries and regions around the world. However, the study of SARS-CoV-2 is still in its infancy, and there is no specific therapeutics. Here, we summarize the genomic characteristics of SARS-CoV-2. In addition, we focus on the mechanisms of SARS-CoV-2 infection, including the roles of angiotensin converting enzyme II (ACE2) in cell entry, COVID-19 susceptibility and COVID-19 symptoms, as well as immunopathology such as antibody responses, lymphocyte dysregulation, and cytokine storm. Finally, we introduce the research progress of animal models of COVID-19, aiming at a better understanding of the pathogenesis of COVID-19 and providing new ideas for the treatment of this contagious disease.

Review: SARS-CoV-2, Cardiovascular Disease, Pathophysiology and Role of ACE2 in Cardiac Injury

The coronavirus disease-2019 (COVID-19), an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has hit the world very hard by affecting millions of people across countries hence posing a major health threat on a global scale. This novel virus is thought to enter and cause infection in its host through the attachment of its structural protein known as the S-glycoprotein to angiotensin-converting enzyme 2 (ACE2). COVID-19 is presented with asymptomatic, mild, or severe pneumonia-like symptoms. During the infection, the cardiovascular system is affected by unknown pathophysiological processes. Among COVID-19 patients, cardiovascular disease (CVD) is resulting into cardiac injury, acute coronary syndrome (ACS), myocardial infarction (MI), arrhythmic infestation and myocarditis. The results of the meta-analysis suggest that CVD and its risk factors are closely related to fatal outcomes in COVID-19 for patients across all ages. Hence, from a cardiovascular standpoint, there are concerns as to whether patients with underlying cardiovascular conditions are at a higher risk of an aggravated COVID-19 infection. Also, as to whether COVID-19 infections induce cardiomyopathies that were not in existence prior to the infection. Nonetheless, much needs to be discovered about the cardiac involvement of this novel coronavirus (nCoV) infection and its relationship with cardiovascular diseases (CVDs). For acute CVD events, the use of antiplatelet agents, β-blockers, angiotensin-converting enzyme inhibitors (ACEIs), angiotensin-receptor blockers (ARBs) and statins are recommended per practice guidelines. Whether the medications which patients used for cardiovascular disease will interfere with the treatment or the outcome of COVID-19, is still unknown. With the invent of vaccines and as new clinical evidences emerging, the diagnosis and treatment may change. The purpose of this concise review is to discuss CVD and related potential disorders in patients with COVID-19 which involves SARS-CoV-2 infection, pathophysiology, role of ACE2 in cardiac injury, possible mechanism of cardiac complications and clinical manifestations.

The Deadly Duo of COVID-19 and Cancer!

As of September 19, 2020, about 30 million people have been infected with the novel corona virus disease 2019 (COVID-19) globally, and the numbers are increasing at an alarming rate. The disease has a tremendous impact on every aspect of life, but one of the biggest, related to human health and medical sciences, is its effect on cancer. Nearly 2% of the total COVID-19 patients prior to May 2020 had cancer, and the statistics are quite frightening as the patient can be referred to as “doubly unfortunate” to suffer from cancer with the added misery of infection with COVID-19. Data regarding the present situation are scarce, so this review will focus on the deadly duo of COVID-19 and cancer. The focus is on molecular links between COVID-19 and cancer as inflammation, immunity, and the role of angiotensin converting enzyme 2 (ACE2). Complications may arise or severity may increase in cancer patients due to restrictions imposed by respective authorities as an effort to control COVID-19. The impact may vary from patient to patient and factors may include a delay in diagnosis, difficulty managing both cancer therapy and COVID-19 at same time, troubles in routine monitoring of cancer patients, and delays in urgent surgical procedures and patient care. The effect of anti-cancer agents on the condition of cancer patients suffering from COVID-19 and whether these anti-cancer agents can be repurposed for effective COVID-19 treatment are discussed. The review will be helpful in the management of deadly duo of COVID-19 and cancer.

ACE2 CONTRIBUTES TO THE NORMAL REGULATION OF ARTERIAL PRESSURE AND IMMUNITY IN FEMALES OF REPRODUCTIVE AGE

Objective: Hypertension and cardiovascular disease are age and sex dependent. These differences may, in part, be mediated by the depressor/pressor balance of the renin angiotensin system. Here we determined the role of angiotensin converting enzyme 2 (ACE2) in the regulation of arterial pressure in females of reproductive age and investigated whether targeting deficits in ACE2-generated angiotensin (Ang)-(1–7) restores the normal regulation of arterial pressure during pregnancy. Design and method: Mean arterial pressure (MAP) was measured via telemetry in 14 week old wild-type (WT) and ACE2 knockout (ACE2-KO) male mice and WT and ACE2-KO female mice receiving vehicle or the MasR agonist, AVE-0991 (24 ug/kg/min s.c) prior to and during pregnancy. FACS analysis was used to determine circulating immune cell activation and infiltration into kidneys (baseline and Gd18) and placentae (Gd18). Results: Basal MAP was lower in WT females than ACE2-KO females, WT males and ACE2-KO males (91 ± 2 vs 100 ± 1, 98 ± 1 and 102 ± 2 mmHg, respectively; all P < 0.05 vs WT female). In ACE2-KO females, AVE-0991 lowered basal MAP by 5 ± 1 mmHg (P = 0.03). In WT females, MAP decreased during pregnancy reaching a nadir at Gd9 before returning to pre-conception levels during late gestation. In contrast, in ACE2-KO mice, MAP increased significantly during late gestation (P < 0.0001 vs WT) and this effect was prevented by AVE-0991 (P < 0.05 vs vehicle). This effect of AVE-0991 on MAP was due to changes in diastolic rather than systolic arterial pressure. ACE2-KO mice had smaller litters but greater birth/pup weight than WT mice. AVE-0991 normalised litter size and birth/pup weight in ACE2-KO mice to that observed in WT mice. Circulating and renal T-regulatory cells were lower in non-pregnant and pregnant female and male ACE2-KO mice than their WT counterparts. Treatment with AVE-0991 did not alter the proportion of T-regulatory cells. Conclusions: These data indicate that ACE2 plays an important role in the regulation of arterial pressure and immunity in females of reproductive age. A corollary of this is that deficits in ACE2-generated Ang-(1–7) may contribute to an increased risk of hypertension in non-pregnant and pregnant premenopausal females and therefore may be a novel therapeutic target.

Novel roles of the renal angiotensin-converting enzyme

The observation that all components of the renin angiotensin system (RAS) are expressed in the kidney and the fact that intratubular angiotensin (Ang) II levels greatly exceed the plasma concentration suggest that the synthesis of renal Ang II occurs independently of the circulating RAS. One of the main components of this so-called intrarenal RAS is angiotensin-converting enzyme (ACE). Although the role of ACE in renal disease is demonstrated by the therapeutic effectiveness of ACE inhibitors in treating several conditions, the exact contribution of intrarenal versus systemic ACE in renal disease remains unknown. Using genetically modified mouse models, our group demonstrated that renal ACE plays a key role in the development of several forms of hypertension. Specifically, although ACE is expressed in different cell types within the kidney, its expression in renal proximal tubular cells is essential for the development of high blood pressure. Besides hypertension, ACE is involved in several other renal diseases such as diabetic kidney disease, or acute kidney injury even when blood pressure is normal. In addition, studies suggest that ACE might mediate at least part of its effect through mechanisms that are independent of the Ang I conversion into Ang II and involve other substrates such as N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP), Ang-(1–7), and bradykinin, among others. In this review, we summarize the recent advances in understanding the contribution of intrarenal ACE to different pathological conditions and provide insight into the many roles of ACE besides the well-known synthesis of Ang II.

The Physiological Mechanisms of the Sex-Based Difference in Outcomes of COVID19 Infection.

The scale of the SARS-CoV-2 pandemic has thrust a spotlight on the sex-based differences in response to viral diseases; morbidity and mortality are greater in men than women. We outline the mechanisms by which being female offers a degree of protection from COVID19, that persists even when confounders such as comorbidities are considered. The physiological and immunological mechanisms are fascinating and range from incomplete X chromosome inactivation of immune genes, a crucial role for angiotensin converting enzyme 2 (ACE2), and regulation of both immune activity and ACE2 by sex steroids. From this flows understanding of why lung and other organs are more susceptible to COVID19 damage in men, and how their distinct immunological landscapes need to be acknowledged to guide prognosis and treatment. Pregnancy, menopause, and hormone replacement therapy bring changed hormonal environments and the need for better stratification in COVID19 studies. We end by noting clinical trials based on increasing estrogens or progesterone or anti-testosterone drugs; excellent examples of translational physiology.

Renin-angiotensin system blockade in the COVID-19 pandemic.

In the early months of the coronavirus disease 2019 (COVID-19) pandemic, a hypothesis emerged suggesting that pharmacologic inhibitors of the renin–angiotensin system (RAS) may increase COVID-19 severity. This hypothesis was based on the role of angiotensin-converting enzyme 2 (ACE2), a counterregulatory component of the RAS, as the binding site for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), allowing viral entry into host cells. Extrapolations from prior evidence led to speculation that upregulation of ACE2 by RAS blockade may increase the risk of adverse outcomes from COVID-19. However, counterarguments pointed to evidence of potential protective effects of ACE2 and RAS blockade with regard to acute lung injury, as well as substantial risks from discontinuing these commonly used and important medications. Here we provide an overview of classic RAS physiology and the crucial role of ACE2 in systemic pathways affected by COVID-19. Additionally, we critically review the physiologic and epidemiologic evidence surrounding the interactions between RAS blockade and COVID-19. We review recently published trial evidence and propose important future directions to improve upon our understanding of these relationships.

ACE2 in the second act of COVID-19 syndrome: Peptide dysregulation and possible correction with oestrogen.

Coronavirus disease 2019 (COVID‐19) has become the most critical pandemic of the 21st Century and the most severe since the 1918 influenza pandemic. Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infects the host by binding to angiotensin‐converting enzyme 2 (ACE2). The role of ACE2 in the pathophysiology of coronavirus disease 2019 (COVID‐19) is a topic of debate, with clinical and experimental evidence indicating a multifaceted relationship between ACE2 activity and disease severity. Here, we review the mechanisms by which the peptidergic substrates and products of ACE and ACE2 contribute to physiological and pathophysiological processes and hypothesise how down‐regulation of ACE2 by SARS‐CoV‐2 cellular entry disrupts homeostasis. A better understanding of the endocrinology of the disease, in particular the neuroendocrinology of ACE2 during COVID‐19, may contribute to the timely design of new therapeutic strategies, including the regulation of ACE2 itself by steroid hormones, to ameliorate the severity of COVID‐19.

Kinins and chymase: the forgotten components of the renin-angiotensin system and their implications in COVID-19 disease.

The unique clinical features of COVID-19 disease present a formidable challenge in the understanding of its pathogenesis. Within a very short time, our knowledge regarding basic physiological pathways that participate in SARS-CoV-2 invasion and subsequent organ damage have been dramatically expanded. In particular, we now better understand the complexity of the renin-angiotensin-aldosterone system (RAAS) and the important role of angiotensin converting enzyme (ACE)-2 in viral binding. Furthermore, the critical role of its major product, angiotensin (Ang)-(1–7), in maintaining microcirculatory balance and in the control of activated proinflammatory and procoagulant pathways, generated in this disease, have been largely clarified. The kallikrein-bradykinin (BK) system and chymase are intensively interwoven with RAAS through many pathways with complex reciprocal interactions. Yet, so far, very little attention has been paid to a possible role of these physiological pathways in the pathogenesis of COVID-19 disease, even though BK and chymase exert many physiological changes characteristic to this disorder. Herein, we outline the current knowledge regarding the reciprocal interactions of RAAS, BK, and chymase that are probably turned-on in COVID-19 disease and participate in its clinical features. Interventions affecting these systems, such as the inhibition of chymase or blocking BKB1R/BKB2R, might be explored as potential novel therapeutic strategies in this devastating disorder.

Mutations in spike protein and allele variations in ACE2 impact targeted therapy strategies against SARS-CoV-2.

Coronavirus disease 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has spread rapidly worldwide with high rates of transmission and substantial mortality. To date, however, no effective treatments or enough vaccines for COVID-19 are available. The roles of angiotensin converting enzyme 2 (ACE2) and spike protein in the treatment of COVID-19 are major areas of research. In this study, we explored the potential of ACE2 and spike protein as targets for the development of antiviral agents against SARS-CoV-2. We analyzed clinical data, genetic data, and receptor binding capability. Clinical data revealed that COVID-19 patients with comorbidities related to an abnormal renin-angiotensin system exhibited more early symptoms and poorer prognoses. However, the relationship between ACE2 expression and COVID-19 progression is still not clear. Furthermore, if ACE2 is not a good targetable protein, it would not be applicable across a wide range of populations. The spike-S1 receptor-binding domain that interacts with ACE2 showed various amino acid mutations based on sequence analysis. We identified two spike-S1 point mutations (V354F and V470A) by receptor-ligand docking and binding enzyme-linked immunosorbent assays. These variants enhanced the binding of the spike protein to ACE2 receptors and were potentially associated with increased infectivity. Importantly, the number of patients infected with the V354F and V470A mutants has increased with the development of the SARS-CoV-2 pandemic. These results suggest that ACE2 and spike-S1 are likely not ideal targets for the design of peptide drugs to treat COVID-19 in different populations.

Role of Angiotensin-Converting Enzyme (ACE) gene polymorphism and ACE activity in predicting outcome after acute myocardial infarction.

The Ace polymorphism had shown association with ACE activity, premature atherosclerosis, myocardial infarction, LV dysfunction, LV remodelling, severity and extent of CAD and mortality after MI. Though ACE I/D polymorphism has been reported to be associated with various cardiovascular diseases it remained a controversial risk factor and studies have presented conflicting results. This study was designed to determine the association between ACE) gene insertion/deletion (I/D) polymorphism, ACE activity and acute STEMI in Indian population and to determine its influence on outcome after acute MI. We investigated 934 patients diagnosed with acute STEMI who underwent thrombolysis. ACE I/D polymorphism was detected by polymerase chain reaction and ACE activity was measured in 615 patients. The prevalence of DD, ID, and II genotypes in our study group were 41.97%, 34.36%, and 23.66% respectively. The ACE polymorphism was not significantly associated with the type of myocardial infarction, the LV ejection fraction, the number of vessels diseased and patency of the vessel after thrombolysis. The polymorphism had no influence on in hospital mortality (P=0.453). The ACE activity also showed no influence on in hospital mortality (P=0.482). The age>60years, Male gender, occluded artery and severe LV dysfunction (LVEF<35%) were predictors of in-hospital mortality on multivariate regression analysis. There was no differences among ACE (I/D) polymorphism observed in STEMI population. Neither ACE I/D polymorphism nor ACE activity predicted in-hospital mortality inpatients admitted with acute STEMI.

The Role of Angiotensin-Converting Enzyme in Immunity: Shedding Light on Experimental Findings

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Immunodeficiency-associated lymphoproliferative disorders and lymphoid neoplasms in post-COVID-19 pandemic era

The 2017revision of WHO Classification of tumors of hematopoietic and lymphoid tissues contains separate chapters on the immunodeficiency-associated lymphoproliferative disorders. In this mini-review, the brief description of pathological, immunophenotypical and clinical features of lymphoid neoplasms associated with primary immune disorders, HIV infection, those arising in post-transplant setting and other lymphoproliferative disorders (excluding those induced by radiation) is given. The heterogeneous spectrum of these lymphoid malignancies is specified by the nature of those factors that are capable to induce immune suppression or chronic antigenic stimulation of immune system. Taking into account the full swing of SARS-CoV-2pandemic and our ignorance of the ability of this virus to induce the sustained stimulation of immune system, we could not exclude the high risk of autoimmune diseases and lymphoid neoplasms in the long-term post-pandemic period. In this context, the role of angiotensin-converting enzyme 2 as well as some recently reported cell receptors for SARS-CoV-2cell entry should be considered as far as some of them (CD147, CD26) could be tumor-associated antigens.

The Controversy on the Role of ACE2 Receptor in COVID-19 Infection: The Protective Shift toward the ACE2 Axis

Background: Angiotensin-converting enzyme 2 (ACE2) is recognized as the main cellular receptor for the new coronavirus, SARS-CoV-2, that facilitates its entry into the host target cell, leading to the fatal viral infection, coronavirus disease 2019 (COVID-19). Thus, it is considered as a main therapeutic target in the SARS-CoV-2 infection. The dual role of ACE2 as a gate for SARS-CoV-2 virus and as a part of lung and multi-organ protection has built a scientific debate that affects the choice of treatments used against COVID-19 patient. ACE2 inhibitors like anti-ACE2 antibodies were first introduced as therapeutic solutions that, theoretically, would decrease the availability of target molecules for SARS-CoV-2 by downregulating ACE2 expression. However, animal studies showed that ACE2 upregulation acts as a counterbalance to the hypertensive pro-inflammatory angiotensin I-converting enzyme (ACE) in the renin–angiotensin system (RAS) and results in a protective role against acute lung injury – a fatal consequence of the disease. The current study tests the effect of ACE2-activating treatments against the outcome of genetic variations in the population that have ACE2-upregulatory effects.&#x0D; Conclusion Despite its role as a receptor for the SARS-CoV-2 virus, experimental studies and the genetic polymorphisms in populations that have ACE2 upregulation revealed a protective role against COVID-19 infection.&#x0D; &#x0D; Key words: ACE2 ACE COVID-19 treatments genetic variations

Advances in the Interaction between Intestinal Microbiota and COVID-19

Coronavirus disease 2019 (COVID-19) is a global epidemic disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Many digestive symptoms have been reported in patients infected with this virus, however, the relationship between the intestinal microbiota and SARS-CoV-2 remains unknown. This review aims to elucidate the interaction between intestinal microbiota and SARS-CoV-2, and review the mechanism of interaction between these two items as well as the effects of probiotics. This review further discusses various studies on gastrointestinal symptoms and changes in intestinal microbiota in COVID-19 patients. To further understand the mechanism, we focused on the role of angiotensin converting enzyme 2 and transmembrane protease serine 2 in this viral infection. There is a correlation between many diseases and dysbiosis of intestinal microbiota. SARS-CoV-2 can lead to dysbiosis of intestinal microbiota through a variety of mechanisms, with a decrease in the abundance and diversity of probiotics and an increase in that of pathogenic bacteria. Dysbiosis of intestinal microbiota results in the translocation of intestinal flora, aggravation of systemic inflammation, and lung injury. Modulating the intestinal microbiota ameliorates digestive symptoms and pathology in infectious respiratory diseases. Intestinal microbiota and SARS-CoV-2 interact through a variety of mechanisms; SARS-CoV-2 can cause dysbiosis of the intestinal microbiota, while dysbiosis of intestinal microbiota, in turn, aggravates COVID-19.

A review on the role of angiotensin-converting enzyme 2 in children with coronavirus disease 2019

With the spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) all over the world, there is an increasing number of children with such infection. Angiotensin-converting enzyme 2 (ACE2), one of the binding sites for SARS-CoV-2 infection in humans, can bind to viral spike proteins, allowing transmembrane serine protease (TMPRSS2) to activate S-protein to trigger infection and induce the production of various inflammatory factors such as interleukin-1, interferon-l, and tumor necrosis factor. Compared with adults, children tend to have lower expression levels of ACE2 and TMPRSS2, which are presumed to be associated with milder symptoms and fewer cases in children. The article summarizes the research advances in the role of ACE2 during SARS-CoV-2 infection, in order to help understand the pathogenic mechanism of SARS-CoV-2 and provide a reference for better development of drugs and vaccines to prevent and treat coronavirus disease 2019 in children.

Clinical characteristics and fatal outcomes of hypertension in patients with severe COVID-19

The aim of this study is to investigate clinical characteristics and fatal outcomes of hypertension as well as the role of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (ACEI/ARB) use in patients with severe coronavirus disease 2019 (COVID-19). A total of 220 (female: 51.8%) patients with severe COVID-19 were included. The mean age of included patients was 59.5 years and 70 (31.8%) patients had a history of hypertension. There were 23 patients (32.9%) receiving ACEI/ARB therapy. Patients with hypertension were older and had more comorbidities, and were more likely to suffer from severe inflammatory response and acute cardiac injury. Moreover, patients with hypertension were associated with significantly higher risk of in-hospital mortality than patients without hypertension. After adjustment of potential confounders, the independent correlation was still observed. In addition, ACEI/ARB users were associated with lower level of high-sensitivity cardiac troponin I and creatinine kinase–myocardial band, and lower risk of acute cardiac injury than ACEI/ARB non-users. In conclusion, patients with hypertension were more likely to suffer from severe inflammatory response, acute cardiac injury and had high risk of in-hospital mortality in severe COVID-19. The use of ACEI/ARB may protect patients with COVID-19 from acute cardiac injury.