Potential Mechanisms Underlying COVID-19-Mediated Central and Peripheral Demyelination: Roles of the RAAS and ADAM-17.

Autor: Oliveira KB; Institute of Biological Sciences and Health, Federal University of Alagoas (UFAL), Av. Lourival de Melo Mota, Km 14, Campus A. C. Simões, Cidade Universitária, Maceió, AL, CEP, 57072-970, Brazil., de Souza FMA; Institute of Biological Sciences and Health, Federal University of Alagoas (UFAL), Av. Lourival de Melo Mota, Km 14, Campus A. C. Simões, Cidade Universitária, Maceió, AL, CEP, 57072-970, Brazil., de Sá LBM; Institute of Biological Sciences and Health, Federal University of Alagoas (UFAL), Av. Lourival de Melo Mota, Km 14, Campus A. C. Simões, Cidade Universitária, Maceió, AL, CEP, 57072-970, Brazil., Pacheco ALD; Institute of Biological Sciences and Health, Federal University of Alagoas (UFAL), Av. Lourival de Melo Mota, Km 14, Campus A. C. Simões, Cidade Universitária, Maceió, AL, CEP, 57072-970, Brazil., Prado MR; Institute of Biological Sciences and Health, Federal University of Alagoas (UFAL), Av. Lourival de Melo Mota, Km 14, Campus A. C. Simões, Cidade Universitária, Maceió, AL, CEP, 57072-970, Brazil., de Sousa Rodrigues CF; Institute of Biological Sciences and Health, Federal University of Alagoas (UFAL), Av. Lourival de Melo Mota, Km 14, Campus A. C. Simões, Cidade Universitária, Maceió, AL, CEP, 57072-970, Brazil., Bassi ÊJ; Institute of Biological Sciences and Health, Federal University of Alagoas (UFAL), Av. Lourival de Melo Mota, Km 14, Campus A. C. Simões, Cidade Universitária, Maceió, AL, CEP, 57072-970, Brazil., Santana-Melo I; Institute of Biological Sciences and Health, Federal University of Alagoas (UFAL), Av. Lourival de Melo Mota, Km 14, Campus A. C. Simões, Cidade Universitária, Maceió, AL, CEP, 57072-970, Brazil., Silva-Júnior A; Institute of Biological Sciences and Health, Federal University of Alagoas (UFAL), Av. Lourival de Melo Mota, Km 14, Campus A. C. Simões, Cidade Universitária, Maceió, AL, CEP, 57072-970, Brazil., Sabino-Silva R; Department of Physiology, Institute of Biomedical Sciences, Federal University of Uberlândia (UFU), Uberlândia, MG, Brazil., Shetty AK; Institute for Regenerative Medicine, Department of Cell Biology and Genetics, Texas A&M University School of Medicine, College Station, TX, USA. akskrs@tamu.edu.; Institute for Regenerative Medicine, Department of Molecular and Cellular Medicine, Texas A&M Health Science Center College of Medicine, College Station, TX, 77843, USA. akskrs@tamu.edu., de Castro OW; Institute of Biological Sciences and Health, Federal University of Alagoas (UFAL), Av. Lourival de Melo Mota, Km 14, Campus A. C. Simões, Cidade Universitária, Maceió, AL, CEP, 57072-970, Brazil. olagidewww@gmail.com.
Jazyk: angličtina
Zdroj: Molecular neurobiology [Mol Neurobiol] 2024 Jul 04. Date of Electronic Publication: 2024 Jul 04.
DOI: 10.1007/s12035-024-04329-8
Abstrakt: Demyelination is among the most conspicuous neurological sequelae of SARS-CoV-2 infection (COVID-19) in both the central (CNS) and peripheral (PNS) nervous systems. Several hypotheses have been proposed to explain the mechanisms underlying demyelination in COVID-19. However, none have considered the SARS-CoV-2's effects on the renin-angiotensin-aldosterone system (RAAS). Therefore, our objective in this review is to evaluate how RAAS imbalance, caused by direct and indirect effects of SARS-CoV-2 infection, could contribute to myelin loss in the PNS and CNS. In the PNS, we propose that demyelination transpires from two significant changes induced by SARS-CoV-2 infection, which include upregulation of ADAM-17 and induction of lymphopenia. Whereas, in the CNS, demyelination could result from RAAS imbalance triggering two alterations: (1) a decrease in angiotensin type II receptor (AT2R) activity, responsible for restraining defense cells' action on myelin; (2) upregulation of ADAM-17 activity, leading to impaired maturation of oligodendrocytes and myelin formation. Thus, we hypothesize that increased ADAM-17 activity and decreased AT2R activity play roles in SARS-CoV-2 infection-mediated demyelination in the CNS.
(© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)
Databáze: MEDLINE
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