Targeting iRhom2/ADAM17 attenuates COVID-19-induced cytokine release from cultured lung epithelial cells.

ABSTRACT: The COVID-19 pandemic, caused by SARS-CoV-2, continues to pose a significant global health challenge, with acute respiratory distress syndrome (ARDS) being a major cause of mortality. Excessive cytokine release (cytokine storm) has been causally related to COVID-19-associated ARDS. While TNF-α inhibitors have shown potential in reducing inflammation, their broad effects on TNF-α signaling, including both pro- and anti-inflammatory pathways, present significant challenges and side effects in clinical use. Therefore, more precise therapeutic targets are urgently needed. ADAM17 is a key enzyme driving cytokine release, but its broad presence complicates direct inhibition. Targeting iRhom2, a regulator specific to immune cells that controls ADAM17's activity, offers a more focused and effectiv

SUBMITTER: Mattos Pereira V 

PROVIDER: S-EPMC11382212 | biostudies-literature | 2024 Sep

REPOSITORIES: biostudies-literature