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Similarities between COVID-19 and systemic sclerosis early vasculopathy: A “viral” challenge for future research in scleroderma

OBJECTIVE: To review similarities between COVID-19 and systemic sclerosis (SSc) early vasculopathy to provide novel insights into both diseases. METHODS: A narrative review of the literature supplemented with expert opinion. RESULTS: There is clear evidence that the endothelium is at the centre stag...

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Detalles Bibliográficos
Autores principales: Matucci-Cerinic, Marco, Hughes, Michael, Taliani, Gloria, Kahaleh, Bashar
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Published by Elsevier B.V. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8280663/
https://www.ncbi.nlm.nih.gov/pubmed/34274540
http://dx.doi.org/10.1016/j.autrev.2021.102899
Descripción
Sumario:OBJECTIVE: To review similarities between COVID-19 and systemic sclerosis (SSc) early vasculopathy to provide novel insights into both diseases. METHODS: A narrative review of the literature supplemented with expert opinion. RESULTS: There is clear evidence that the endothelium is at the centre stage in SSc and COVID-19, with endothelial cell activation/injury and dysfunction creating the crucial evolving step in the pathogenesis of both diseases. The angiotensin system has also been implicated in the early stages of both COVID-19 and SSc. Autoptic studies provide novel insights into the effects of SARS-CoV-2 on the endothelium. Normal endothelium and endothelial dysfunction in COVID-19 and SSc are discussed. It is debated whether SARS-CoV-2 infection triggers autoimmunity with production of autoantibodies which is of mechanistic interest because other viral illnesses are potentially involved in endothelial dysfunction and in SSc pathogenesis. CONCLUSION: COVID-19 is due to a direct assault of SARS-CoV-2 on the vascular system as an acute infection, whereas SSc remains a chronic/sub-acute autoimmune disease of largely unknown etiology Further study and exploration of the SARS-CoV-2 pathogenic mechanisms might provide further useful milestones in the understanding of the early SSc pathogenesis.