Authors
Xu Yang, Yage Sun, Yanbo Zhu, Liuying Zheng, Shan Liu, Kai Hou, Ru Zhao, Lu Cao, Hongliang Cong
Published in
Journal of materials chemistry. B. Sep 25, 2026. Epub Sep 25, 2026.
Abstract
Myocardial infarction (MI) triggers severe oxidative stress and ferroptosis, leading to progressive cardiomyocyte death and impaired cardiac function. Inhibiting ferroptosis in ischemic myocardium with Ferrostatin-1 (Fer-1) shows potential in reducing oxidative stress and preserving cardiac function after MI. To address the challenges of Fer-1's poor water solubility and low cardiac retention, we developed an innovative injectable hydrogel system for synchronized antioxidant and ferroptosis-inhibiting therapy. Fer-1 was first encapsulated into liposomes (Lipo@Fer-1) to enhance its solubility and bioavailability. Then the liposomes were integrated into a degradable hydrogel composed of oxidized dextran and thiol-modified poly (γ-glutamic acid) (PS-OD-Lipo@Fer-1). The hydrogel aims to prolong the retention of Fer-1 around the infarct area while leveraging the inherent ROS-scavenging ability of the hydrogel. In experiments in vitro, Lipo@Fer-1 demonstrated superior protective effects against H2O2-induced oxidative damage in H9C2 cells compared to free Fer-1. In a model of acute MI in vivo, the PS-OD-Lipo@Fer-1 hydrogel significantly improved cardiac function, decreased apoptosis and fibrosis, and facilitated angiogenesis. These are achieved by efficiently and securely prolonging the duration of Fer-1 presence around the infarction area to mitigate ferroptosis in cardiomyocytes, ROS reduction and providing structural support with hydrogel after MI.
PMID:
42831493
Bibliographic data and abstract were imported from PubMed on 05 Oct 2026.
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