A galunisertib-loaded microneedle patch improved long-term cardiac function and reduced cardiac fibrosis in a rat model of myocardial infarction by inhibiting TGF-β.
Does a galunisertib-loaded microneedle patch improve cardiac function and reduce fibrosis in a rat model of myocardial infarction?
A galunisertib-loaded microneedle patch provides sustained local delivery of an antifibrotic drug, improving cardiac function and reducing fibrosis in a rat model of myocardial infarction.
Uncontrolled and excessive fibrosis after myocardial infarction (MI) in the peri-infarct zone leads to left ventricular remodeling and deterioration of cardiac function. Inhibiting fibroblast activation during the mature phase of cardiac repair improves cardiac remodeling and function after MI. Here, we engineered a biocompatible microneedle (MN) patch using gelatin methacryloyl and loaded it with galunisertib, a transforming growth factor-beta (TGF-β)-specific inhibitor, to treat excessive cardiac fibrosis after MI. The MN patch could sustainably release galunisertib for more than 2 weeks and provide mechanical support for the fragile ventricular wall. After being applied to a rat model of MI, the galunisertib-loaded MN patch improved long-term cardiac function and reduced cardiac fibrosis by effectively inhibiting TGF-β depending on fibroblast activation. This strategy shows the potential of the MN patch as an advanced platform to locally deliver direct antifibrotic drugs to prevent myocardial fibrosis for the treatment of MI and the promotion of cardiac repair.
Chen et al. (Mon,) conducted a other in Myocardial Infarction. Galunisertib-loaded gelatin methacryloyl hydrogel microneedle patch was evaluated on Cardiac function and cardiac fibrosis. A galunisertib-loaded microneedle patch improved long-term cardiac function and reduced cardiac fibrosis in a rat model of myocardial infarction by inhibiting TGF-β.