PRMT9 expression is significantly upregulated in human and murine peripheral blood mononuclear cells during the acute phase of myocardial infarction (MI).
Macrophage-specific PRMT9 deficiency exacerbates post-MI cardiac damage by promoting M1-like proinflammatory polarization, while its overexpression facilitates inflammation resolution and functional recovery.
Mechanistically, PRMT9 catalyzes the symmetric dimethylation of STAT1 at residues R588 and R736, triggering its ubiquitination and subsequent selective autophagic degradation via the p62/NDP52 pathway.
Pharmacological inhibition of STAT1 with fludarabine can rescue the adverse cardiac phenotype induced by PRMT9 loss, highlighting a potential translational pathway for clinical intervention.
Background
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This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
