Affiliations 

  • 1 Institute of Pharmaceutical Sciences, Guru Ghasidas University (A Central University), Bilaspur, Chhattisgarh, 495 009, India
  • 2 Department of Pharmaceutical Chemistry, College of Pharmacy, Prince Sattam Bin Abdulaziz University, P.O. Box No. 173, Al-Kharj, 11942, Kingdom of Saudi Arabia
  • 3 Department of Pharmacology, College of Medicine, Al Imam Bin Saud Islamic University, Riyadh, 13314, Kingdom of Saudi Arabia
  • 4 School of Pharmacy, Faculty of Health and Medical Sciences, Taylor's University, 47500, Subang Jaya, Selangor, Malaysia
  • 5 Department of Pharmaceutics, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, 110062, India. prashantdops@gmail.com
  • 6 Institute of Pharmaceutical Sciences, Guru Ghasidas University (A Central University), Bilaspur, Chhattisgarh, 495 009, India. harishdops@yahoo.co.in
Pharmacol Rep, 2021 Dec;73(6):1539-1550.
PMID: 34176080 DOI: 10.1007/s43440-021-00303-6

Abstract

Angiotensin-converting enzyme (ACE) and its homologue, ACE2, are commonly allied with hypertension, renin-angiotensin-aldosterone system pathway, and other cardiovascular system disorders. The recent pandemic of COVID-19 has attracted the attention of numerous researchers on ACE2 receptors, where the causative viral particle, SARS-CoV-2, is established to exploit these receptors for permitting their entry into the human cells. Therefore, studies on the molecular origin and pathophysiology of the cell response in correlation to the role of ACE2 receptors to these viruses are bringing novel theories. The varying level of manifestation and importance of ACE proteins, underlying irregularities and disorders, intake of specific medications, and persistence of assured genomic variants at the ACE genes are potential questions raising nowadays while observing the marked alteration in response to the SARS-CoV-2-infected patients. Therefore, the present review has focused on several raised opinions associated with the role of the ACE2 receptor and its impact on COVID-19 pathogenesis.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.