Details

Autor(en) / Beteiligte

• Oliveira, Kellysson Bruno
• de Souza, Fernanda Maria Araujo
• de Sá, Letícia Barros Maurício
• Pacheco, Amanda Larissa Dias
• Prado, Mariana Reis
• de Sousa Rodrigues, Célio Fernando
• Bassi, Ênio José
• Santana-Melo, Igor
• Silva-Júnior, Abelardo
• Sabino-Silva, Robinson
• Shetty, Ashok K
• de Castro, Olagide Wagner

Titel

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

Ist Teil von

• Molecular neurobiology, 2024-07

Ort / Verlag

United States

Erscheinungsjahr

2024

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• 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.