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作 者:Konstantinos I Papadopoulos Alexandra Papadopoulou Tar Choon Aw
机构地区:[1]Department of R and D,THAI StemLife,Bangkok 10310,Thailand [2]Department of Occupational and Environmental Health Services,Feelgood Lund,Lund 223-63,Skåne,Sweden [3]Department of Laboratory Medicine,Changi General Hospital,Singapore 529889,Singapore [4]Department of Medicine,National University of Singapore,Singapore 119228,Singapore
出 处:《World Journal of Experimental Medicine》2025年第2期246-252,共7页世界实验医学杂志(英文)
摘 要: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.
关 键 词:Angiotensin converting enzyme inhibitors Angiotensin II type 1 receptor blocker COVID-19 MicroRNA Mineralocorticosteroid receptor antagonists MicroRNA-155 Renin-angiotensin system inhibitors SARS-CoV-2 Sodium-glucose transporter 2
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