Full text is available at the source.
MicroRNA-328, a Potential Anti-Fibrotic Target in Cardiac Interstitial Fibrosis
MicroRNA-328 as a Possible Target to Reduce Scarring in Heart Tissue
AI simplified
Abstract
miR-328 was significantly upregulated in the border zone of infarcted myocardium in mice.
- Deregulated myocardial fibrosis is linked to various heart conditions and is considered a major cause of heart disease.
- TGFβRIII was downregulated while TGF-β1 was upregulated in the context of increased cardiac fibrosis.
- miR-328 may stimulate TGF-β1 signaling and promote collagen production in heart cells.
- The pro-fibrotic effects of miR-328 are associated with its targeting of TGFβRIII.
- Treatment with miR-328 antisense significantly reduced cardiac fibrosis in the infarcted heart.
AI simplified