Patients with coronavirus disease 2019 (COVID-19) can develop acute respiratory distress syndrome (ARDS), which has been linked to poor prognosis and is a major contributor to patient death. A better understanding of the pathophysiology of COVID-19-related ARDS would benefit early, precise treatment.

Cell death plays a major role in ARDS pathogenesis.

While apoptosis in acute lung injury is well studied, newly identified cell death signaling has drawn attention as a potential mediator of ARDS.

Necroptosis, a caspase-independent form of necrosis involving receptor-interacting kinase 3 (RIPK-3), has been implicated in ARDS development with sepsis and trauma.

Since this highly regulated cell death signaling leads to rupture of the plasma membrane and release of damage-associated molecular patterns, necroptosis may be a therapeutic target for ARDS.

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