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Angiotensin Converting Enzyme 2 (ACE2): Cellular and Clinical Aspects of an Underused Pharmacological Target

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 January 2021) | Viewed by 14073

Special Issue Editor

Prof. Dr. Catalin Filipeanu

E-Mail Website
Guest Editor
Department of Pharmacology, College of Medicine, Howard University, Washington, DC 20059, USA
Interests: GPCR (G protein-coupled receptors); orphan GPCR; Angiotensin type I receptor (AT1R); Angiotensin Converting Enzyme 2 (ACE2); Rab GTP-ases; cannabinoid receptors

Special Issue Information

Dear Colleagues,

The angiotensin converting enzyme 2 (ACE2) has been identified as a new member of the renin–angiotensin–aldosterone system at beginning of the millennium. Since then, its significant role (putatively via generation of angiotensin(1–7) and activation of MAS1 receptor) in counteracting the pathologic cardiovascular activities of angiotensin II has been demonstrated. Furthermore, ACE2 has been shown to be the cellular receptor for several coronaviruses, including SARS and COVID-19. In addition, recently, an association of ACE2 with other pathologies such Alzheimer’s Disease, neuropsychiatric disorders, regulation of neutral amino acids trafficking, and others has been proposed. However, the therapeutic potential of ACE2 is still quite undeveloped, mainly because of a lack of specific compounds. Recombinant ACE2 (GSK2586881) had been recently abandoned by GlaxoSmithKline, whereas the effects of the only available enzyme activator, diminazene aceturate, are still not fully understood.

The main aim of this Specific Issue is to provide classic and novel views on the cellular and pathological regulation of ACE2 functions which will hopefully accelerate the discovery of new pharmacological tools for this underused target.

Prof. Dr. Catalin Filipeanu
Guest Editor

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Keywords

  • angiotensin converting enzyme 2
  • angiotensin(1-7)
  • angiotensin II
  • MAS1
  • angiotensin type 1 receptor
  • enzyme-receptor interactions
  • collectrin
  • cardiovascular diseases
  • coronavirus receptor

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Published Papers (3 papers)

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Research

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13 pages, 2610 KiB  
Article
Activation of Kinin B1R Upregulates ADAM17 and Results in ACE2 Shedding in Neurons
by Rohan Umesh Parekh and Srinivas Sriramula
Int. J. Mol. Sci. 2021, 22(1), 145; https://doi.org/10.3390/ijms22010145 - 25 Dec 2020
Cited by 11 | Viewed by 3472
Abstract
Angiotensin converting enzyme 2 (ACE2) is a critical component of the compensatory axis of the renin angiotensin system. Alterations in ACE2 gene and protein expression, and activity mediated by A Disintegrin And Metalloprotease 17 (ADAM17), a member of the “A Disintegrin And Metalloprotease” [...] Read more.
Angiotensin converting enzyme 2 (ACE2) is a critical component of the compensatory axis of the renin angiotensin system. Alterations in ACE2 gene and protein expression, and activity mediated by A Disintegrin And Metalloprotease 17 (ADAM17), a member of the “A Disintegrin And Metalloprotease” (ADAM) family are implicated in several cardiovascular and neurodegenerative diseases. We previously reported that activation of kinin B1 receptor (B1R) in the brain increases neuroinflammation, oxidative stress and sympathoexcitation, leading to the development of neurogenic hypertension. We also showed evidence for ADAM17-mediated ACE2 shedding in neurons. However, whether kinin B1 receptor (B1R) activation has any role in altering ADAM17 activity and its effect on ACE2 shedding in neurons is not known. In this study, we tested the hypothesis that activation of B1R upregulates ADAM17 and results in ACE2 shedding in neurons. To test this hypothesis, we stimulated wild-type and B1R gene-deleted mouse neonatal primary hypothalamic neuronal cultures with a B1R-specific agonist and measured the activities of ADAM17 and ACE2 in neurons. B1R stimulation significantly increased ADAM17 activity and decreased ACE2 activity in wild-type neurons, while pretreatment with a B1R-specific antagonist, R715, reversed these changes. Stimulation with specific B1R agonist Lys-Des-Arg9-Bradykinin (LDABK) did not show any effect on ADAM17 or ACE2 activities in neurons with B1R gene deletion. These data suggest that B1R activation results in ADAM17-mediated ACE2 shedding in primary hypothalamic neurons. In addition, stimulation with high concentration of glutamate significantly increased B1R gene and protein expression, along with increased ADAM17 and decreased ACE2 activities in wild-type neurons. Pretreatment with B1R-specific antagonist R715 reversed these glutamate-induced effects suggesting that indeed B1R is involved in glutamate-mediated upregulation of ADAM17 activity and ACE2 shedding. Full article
(This article belongs to the Special Issue Angiotensin Converting Enzyme 2 (ACE2): Cellular and Clinical Aspects of an Underused Pharmacological Target)
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Review

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10 pages, 1559 KiB  
Review
ERAP1 and ERAP2 Enzymes: A Protective Shield for RAS against COVID-19?
by Silvia D’Amico, Patrizia Tempora, Valeria Lucarini, Ombretta Melaiu, Stefania Gaspari, Mattia Algeri and Doriana Fruci
Int. J. Mol. Sci. 2021, 22(4), 1705; https://doi.org/10.3390/ijms22041705 - 8 Feb 2021
Cited by 17 | Viewed by 3528
Abstract
Patients with coronavirus disease 2019 (COVID-19) have a wide variety of clinical outcomes ranging from asymptomatic to severe respiratory syndrome that can progress to life-threatening lung lesions. The identification of prognostic factors can help to improve the risk stratification of patients by promptly [...] Read more.
Patients with coronavirus disease 2019 (COVID-19) have a wide variety of clinical outcomes ranging from asymptomatic to severe respiratory syndrome that can progress to life-threatening lung lesions. The identification of prognostic factors can help to improve the risk stratification of patients by promptly defining for each the most effective therapy to resolve the disease. The etiological agent causing COVID-19 is a new coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that enters cells via the ACE2 receptor. SARS-CoV-2 infection causes a reduction in ACE2 levels, leading to an imbalance in the renin-angiotensin system (RAS), and consequently, in blood pressure and systemic vascular resistance. ERAP1 and ERAP2 are two RAS regulators and key components of MHC class I antigen processing. Their polymorphisms have been associated with autoimmune and inflammatory conditions, hypertension, and cancer. Based on their involvement in the RAS, we believe that the dysfunctional status of ERAP1 and ERAP2 enzymes may exacerbate the effect of SARS-CoV-2 infection, aggravating the symptomatology and clinical outcome of the disease. In this review, we discuss this hypothesis. Full article
(This article belongs to the Special Issue Angiotensin Converting Enzyme 2 (ACE2): Cellular and Clinical Aspects of an Underused Pharmacological Target)
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Other

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6 pages, 519 KiB  
Commentary
Acute Kidney Injury in SARS-CoV-2 Infection: Direct Effect of Virus on Kidney Proximal Tubule Cells
by Manoocher Soleimani
Int. J. Mol. Sci. 2020, 21(9), 3275; https://doi.org/10.3390/ijms21093275 - 5 May 2020
Cited by 62 | Viewed by 6428
Abstract
Coronaviruses (CoVs), including Severe Acute Respiratory Syndrome (SARS), Middle East Respiratory Syndrome (MERS), and the novel coronavirus disease-2 (SARS-CoV-2) are a group of enveloped RNA viruses that cause a severe respiratory infection which is associated with a high mortality [...] Full article
(This article belongs to the Special Issue Angiotensin Converting Enzyme 2 (ACE2): Cellular and Clinical Aspects of an Underused Pharmacological Target)
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