Cardiomyocyte Derived miR-328 Promotes Cardiac Fibrosis by Paracrinely Regulating Adjacent Fibroblasts

Elevated expression of miR-328 is associated with increased cardiac fibrosis in transgenic mice.

• Histological examination revealed progressive fibrosis in mice overexpressing cardiomyocyte-specific miR-328.
• Enhanced collagen deposition in these mice was linked to activation of the TGF-β1 signaling pathway.
• Knockdown of endogenous miR-328 in these mice reduced cardiac fibrosis, indicating its role in fibrogenesis.
• In co-culture experiments, cardiac fibroblasts exhibited increased miR-328 expression when exposed to cardiomyocytes expressing miR-328 mimics.
• The pro-fibrotic effect of miR-328 in cardiac fibroblasts was reversed by the use of a miR-328 inhibitor.

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