The Link Between Heat Shock Proteins, Renin-Angiotensin System, and the Coagulation Cascade in the Pathogenesis of the Coronavirus-19 Disease.
Adv Exp Med Biol
; 2022 Jul 27.
Article
in English
| MEDLINE | ID: covidwho-2279272
ABSTRACT
INTRODUCTION:
Understanding the pathogenesis of COVID-19 is integral for its successful treatment.METHODS:
Available literature on the relationship between COVID-19, heat shock proteins (HSP), and the renin-angiotensin-aldosterone (RAAS) system were searched and used to hypothesize how HSP can be targeted in COVID-19.RESULTS:
During SARS-CoV-2 cellular entry, the ACE-2 receptor is downregulated. This leads to the augmentation of angiotensin-2/AT1 receptor axis along with attenuation of the ACE-2/angiotensin1-7/Mas axis. Heat shock proteins are key stabilizing molecules in various pathways.In the heart and vessels, HSP-90 and HSP-60 can facilitate angiotensin-2-mediated myocardial injury and endothelial cell activation. HSP-60-TLR4/CD14 complex formation stabilizes IκB-kinase (IKK) potentiating NF-κB activation. HSPs in lungs and kidneys have antioxidant, vasodilatory, and anti-inflammatory actions and may be protective against the effects of RAAS. Stress-induced HSP-70 has a role in complement-mediated microvascular injury such as has been demonstrated in COVID-19. SARS-CoV-2 can induce autophagy via Beclin-1 and ER (endoplasmic reticular) stress via BIP. These two can be potential targets in the HSP environment.CONCLUSION:
Various HSP molecules can modulate the effects of the renin-angiotensin-aldosterone (RAAS) system and thus may have a potential role in the pathogenesis of COVID-19.
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Language:
English
Year:
2022
Document Type:
Article
Affiliation country:
5584_2022_735
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