The abstract is read at the publisher; the summary is JClub's.
CCL17 signaling through CCR4 attenuates transverse aortic constriction–induced cardiac remodeling in mice, with CCL17 augmentation reducing systolic dysfunction, hypertrophy, and fibrosis.
- Why it matters: CCL17 is linked to adverse remodeling after other cardiac injuries, but its role during sustained mechanical pressure overload—and the fibroblast pathway involved—was unclear.
- What they did: The study combined serum proteomics and human myocardial measurements with mouse transverse aortic constriction using global Ccl17 deletion or adeno-associated virus–mediated CCL17 augmentation, plus fibroblast transcriptomics and CCR4/EGR1/IGFBP6 perturbation.
- The result: IGFBP6 was identified as a downstream mediator: CCL17 lowered fibroblast IGFBP6 and alpha-smooth muscle actin via CCR4-dependent EGR1 suppression, and fibroblast-directed Igfbp6 silencing improved function and reduced hypertrophy and fibrosis in Ccl17-deficient mice.
The findingWhy it mattersWhat they didThe result
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