Inhibiting the cGAS-STING pathway in myeloid cells effectively improves myocardial healing related to TET2 deficiency-induced DNA damage response

Abstract

Myeloid-specific Tet2 depletion promotes neutrophil expansion upon myocardium infarction (MI);

Tet2-deficient myeloid cells exhibit increased genome instability and cGASSTING overactivation;

STING antagonist H-151 treatment reduces neutrophil expansion in Tet2- deficient mice after MI and mitigates deleterious cardiac outcomes.

Keywords

cGAS-STING / epigenetics / myocardial repair / TET2

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2024 The Author(s). Clinical and Translational Medicine published by John Wiley & Sons Australia, Ltd on behalf of Shanghai Institute of Clinical Bioinformatics.