IRF7 Expression Drives Instability in Atherosclerotic Plaques
Single-cell reanalysis identifies IRF7 as a master regulator driving smooth muscle cell transdifferentiation into pro-inflammatory, macrophage-like cells in atherosclerotic plaques. SMC-specific Irf7 knockdown in ApoE−/− mice reduced plaque progression, necrotic core formation, and improved fibrous cap stability, while IRF7 was elevated in unstable human plaques, supporting translational potential.
Why it mattersIRF7 upregulation in unstable atherosclerotic plaques suggests targeting IRF7 could prioritize therapeutic development to stabilize lesions.