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Publications

Letter Epublish 1 citation

PubMed: 40546676 DOI: 10.5493/wjem.v15.i2.100748

MicroRNA-155 modulation by renin-angiotensin system inhibitors may underlie their enigmatic role in COVID-19.

World J Exp Med 15(2):100748

Authors: Konstantinos I Papadopoulos, Alexandra Papadopoulou, Tar Choon Aw

Affiliations

  • Department of R and D, THAI StemLife, Bangkok 10310, Thailand.
  • Department of Occupational and Environmental Health Services, Feelgood Lund, Lund 223-63, SkÃ¥ne, Sweden.
  • Department of Laboratory Medicine, Changi General Hospital, Singapore 529889, Singapore.
  • Department of Medicine, National University of Singapore, Singapore 119228, Singapore.

Abstract

Severe acute respiratory coronavirus-2 (SARS-CoV-2) infection course differs between the young and healthy and the elderly with co-morbidities. In the latter a potentially lethal coronavirus disease 2019 (COVID-19) cytokine storm has been described with an unrestrained renin-angiotensin (Ang) system (RAS). RAS inhibitors [Ang converting enzyme inhibitors and Ang II type 1 receptor (AT1R) blockers] while appearing appropriate in COVID-19, display enigmatic effects ranging from protection to harm. MicroRNA-155 (miR-155)-induced translational repression of key cardiovascular (CV) genes (i.e., AT1R) restrains SARS-CoV-2-engendered RAS hyperactivity to tolerable and SARS-CoV-2-protective CV phenotypes supporting a protective erythropoietin (EPO) evolutionary landscape. MiR-155's disrupted repression of the AT1R 1166C-allele associates with adverse CV and COVID-19 outcomes, confirming its decisive role in RAS modulation. RAS inhibition disrupts this miR-155-EPO network by further lowering EPO and miR-155 in COVID-19 with co-morbidities, thereby allowing unimpeded RAS hyperactivity to progress precariously. Current pharmacological interventions in COVID-19 employing RAS inhibition should consider these complex but potentially detrimental miR-155/EPO-related effects.

MeSH

Coronavirus, Sars-Cov-2, Micrornas, Repression, Psychology, Renin, Angiotensins, Covid-19, Morbidity, Renin-Angiotensin System