The abstract is read at the publisher; the summary is JClub's.
MOF is increased in aortic monocyte/macrophages in human abdominal aortic aneurysms and is linked to inflammatory transcriptional programs, with TNF-α driving MOF induction.
- Why it matters: AAA formation involves an imbalance of macrophage inflammatory states, but the molecular regulators of macrophage-driven inflammation and aneurysm progression are not well defined.
- What they did: Single-cell RNA sequencing assessed MOF expression in human AAA versus control tissues, while mice used Ang II or topical porcine pancreatic elastase AAA models with myeloid-specific MOF depletion (Mof f/f Lyz2 Cre+) or MG-149 inhibition; flow cytometry and chromatin immunoprecipitation measured macrophage phenotype and H4K16ac.
- The result: In both elastase- and Ang II-induced AAA models, MOF pathway inhibition preserved macrophage function, reduced elastin fragmentation, attenuated aortic inflammation, and markedly reduced AAA development.
The findingWhy it mattersWhat they didThe result
AI summary of the abstract · may contain errors · not medical advice · read the paper.