Inflamasoma, piroptosis y su posible relación con la fisiopatología de la COVID-19. / Inflammation, pyroptosis and its possible relation to the physiopathology of COVID-19.

Palabras clave: inflamasoma, piroptosis, inmunidad innata, fisiopatología, COVID-19, inflammasome, pyroptosis, innate immunity, physiopathology, COVID-19.



SARS-CoV-2 es el agente causal de la pandemia actual de la enfermedad por coronavirus 2019 (COVID-19). Al igual que otros coronavirus respiratorios, el SARS-CoV-2 se transmite principalmente a través de gotitas respiratorias liberadas de una persona infectada. La fisiopatología de la infección por SARS-CoV-2 es semejante a la de la infección por SARS-CoV, con respuestas inflamatorias agresivas lo que genera fuertes daños a las vías respiratorias. En esta revisión abordamos la importancia de la respuesta inmunitaria innata en la fisiopatología de la COVID-19, con especial énfasis en la activación del inflamasoma y la consecuente muerte celular por piroptosis, dos elementos esenciales que podrían explicar la exacerbada respuesta inflamatoria que se observa en algunos pacientes.


SARS-CoV-2 is the causal agent of the current 2019 coronavirus disease pandemic (COVID-19). Like other respiratory coronaviruses, SARSCoV-2 is transmitted primarily through respiratory droplets released from an infected person. The pathophysiology of SARS-CoV-2 infection is similar to that of SARS-CoV infection, with aggressive inflammatory responses resulting in severe damage to the respiratory tract. In this review we address the importance of the innate immune response in the physiopathology of COVID-19 with special emphasis on the activation of the inflammasome and the consequent cell death by pyroptosis, two essential elements that could explain the exacerbated inflammatory response observed in some patients.


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Cómo citar
Pedreáñez, A., Mosquera, J., & Muñoz, N. (2021). Inflamasoma, piroptosis y su posible relación con la fisiopatología de la COVID-19. / Inflammation, pyroptosis and its possible relation to the physiopathology of COVID-19. Investigación Clínica, 61(3), 283-293.