tetano
Editor, Senior Moderator
World J Exp Med
. 2025 Jun 20;15(2):100748.
doi: 10.5493/wjem.v15.i2.100748. MicroRNA-155 modulation by renin-angiotensin system inhibitors may underlie their enigmatic role in COVID-19
Konstantinos I Papadopoulos[SUP] 1 [/SUP], Alexandra Papadopoulou[SUP] 2 [/SUP], Tar Choon Aw[SUP] 3 4 [/SUP]
Affiliations
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.
Keywords: Angiotensin II type 1 receptor blocker; Angiotensin converting enzyme inhibitors; COVID-19; MicroRNA; MicroRNA-155; Mineralocorticosteroid receptor antagonists; Renin-angiotensin system inhibitors; SARS-CoV-2; Sodium-glucose transporter 2.
. 2025 Jun 20;15(2):100748.
doi: 10.5493/wjem.v15.i2.100748. MicroRNA-155 modulation by renin-angiotensin system inhibitors may underlie their enigmatic role in COVID-19
Konstantinos I Papadopoulos[SUP] 1 [/SUP], Alexandra Papadopoulou[SUP] 2 [/SUP], Tar Choon Aw[SUP] 3 4 [/SUP]
Affiliations
- PMID: 40546676
- PMCID: PMC12019617
- DOI: 10.5493/wjem.v15.i2.100748
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.
Keywords: Angiotensin II type 1 receptor blocker; Angiotensin converting enzyme inhibitors; COVID-19; MicroRNA; MicroRNA-155; Mineralocorticosteroid receptor antagonists; Renin-angiotensin system inhibitors; SARS-CoV-2; Sodium-glucose transporter 2.