Il Ruolo chiave dell'annessina A2 e della plasmina nella fisiopatologia del COVID -19 presentazione clinica e risultati

Contenuto principale dell'articolo

Asiya Kamber Zaidi
Sunny Dawoodi
Matteo Pirro
Manuel Monti
Puya Dehgani Mobaraki

Abstract

La pandemia della malattia da Coronavirus 2019 (COVID-19) è diventata una crisi sanitaria globale determinante con un tasso di trasmissione eccezionalmente alto che causa morbilità e mortalità significative.


Studi recenti hanno riportato pazienti che presentavano disturbi della coagulazione e malattia tromboembolica successivamente risultati positivi al coronavirus.


In questo articolo, abbiamo discusso la recente tendenza nella sintomatologia di covid19 inclusa la trombosi microvascolare e il potenziale ruolo chiave di proteine come annessina A2, plasmina, recettori ACE-2 e canali ENaC nella fisiopatologia della malattia.


Le interazioni tra queste molecole e le proteine virali potrebbero svolgere un ruolo nella presentazioe tromboembolica della malattia e spiegare la morbilità selettiva nei pazienti con condizioni ci comorbidità.


È stato anche proposto un modello di lavoro schematico che aiuterà i lettori a comprendere queste interazioni biomolecolari chiave che influenzano la probabile fisiopatologia a livello di recettore cellulare.


Questo articolo farà anche luce sui polimorfismi genetici nei recettori ACE-2 e annessina A2, suggerendo una possibilità di ampia diversità nella presentazione clinica e gravità della malattia in tutto il mondo.


Studi basati sull'evidenza potrebbero guidare nell'identificazione di potenziali terapie e opzioni di trattamento per COVID-19

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[1]
Kamber Zaidi, A., Dawoodi, S., Pirro, M., Monti, M. e Dehgani Mobaraki, P. 2020. Il Ruolo chiave dell’annessina A2 e della plasmina nella fisiopatologia del COVID -19: presentazione clinica e risultati. Italian Journal of Prevention, Diagnostic and Therapeutic Medicine. 3, 4 (set. 2020), 16-25. DOI:https://doi.org/10.30459/2020-24.
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Review

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