COVID-19 and hypertension: is the HSP60 culprit for the severe course and worse outcome?

Autor: Hrvoje Jakovac
Rok vydání: 2020
Předmět:
0301 basic medicine
Physiology
severity
Disease
030204 cardiovascular system & hematology
Mitochondrion
0302 clinical medicine
Mizoribine
Prognosis
Host-Pathogen Interactions
HSP60
Inflammation Mediators
BIOMEDICINA I ZDRAVSTVO. Temeljne medicinske znanosti
Coronavirus Infections
mizoribine
Cardiology and Cardiovascular Medicine
BIOMEDICINA I ZDRAVSTVO. Kliničke medicinske znanosti. Infektologija
Immunosuppressive Agents
Perspectives
Signal Transduction
medicine.drug
animal structures
hypertension
Pneumonia
Viral
Proinflammatory cytokine
Betacoronavirus
03 medical and health sciences
Physiology (medical)
Heat shock protein
medicine
Animals
Humans
Pandemics
SARS-CoV-2
business.industry
BIOMEDICINE AND HEALTHCARE. Basic Medical Sciences
fungi
COVID-19
Chaperonin 60
BIOMEDICINE AND HEALTHCARE. Clinical Medical Sciences. Infectology
medicine.disease
COVID-19 Drug Treatment
030104 developmental biology
Proteostasis
Immunology
Ribonucleosides
Cytokine storm
business
Zdroj: American Journal of Physiology-Heart and Circulatory Physiology
Volume 319
Issue 4
ISSN: 1522-1539
0363-6135
Popis: COVID-19 and hypertension: is the HSP60 culprit for the severe course and worse outcome? Am J Physiol Heart Circ Physiol 319: H793–H796, 2020. First published September 4, 2020 ; doi:10.1152/ajpheart.00506.2020.—The 60-kDa heat shock protein (HSP60) is a chaperone essential for mitochondrial proteostasis ensuring thus sufficient aerobic energy production. In pathological conditions, HSP60 can be translocated from the mitochondria and excreted from the cell. In turn, the extracellular HSP60 has a strong ability to trigger and enhance inflammatory response with marked proinflammatory cytokine induction, which is mainly mediated by Toll-like receptor binding. Previous studies have found increased circulating levels of HSP60 in hypertensive patients, as well as enhanced HSP60 expression and membrane translocation in the hypertrophic myocardium. These observations are of particular interest, since they could provide a possible pathophysiological explanation of the severe course and worse outcome of severe acute respiratory syndrome coronavirus 2 infection in hypertensive patients, repeatedly reported during the recent coronavirus disease 2019 (COVID-19) pandemic and related to hyperinflammatory response and cytokine storm development during the third phase of the disease. In this regard, pharmacological inhibition of HSP60 could attract attention to potentially ameliorate inappropriate inflammatory reaction in severe COVID-19 patients. Among HSP60 antagonizing drugs, mizoribine is the most intriguing, since it is clinically approved and exerts antiviral activity. However, this topic requires to be further scrutinized.
Databáze: OpenAIRE
Externí odkaz: