ArticleInternational journal of nanomedicine2026
Targeted Delivery of Schisandrin A to Cardiac Endothelium Alleviates Myocardial Ischemia-Reperfusion Injury via Suppression of Ferroptosis.
Article in International journal of nanomedicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Purpose: Myocardial microvascular injury plays a critical role in myocardial ischemia‑reperfusion injury (MI/RI), and ferroptosis has emerged as an important contributor to cardiac damage. Although Schizandrin A (Sch) possesses cardioprotective effects, its clinical application is limited by poor stability and low bioavailability. This study aimed to develop a CMEC‑targeted delivery system for Sch and evaluate its ability to attenuate ferroptosis in cardiac microvascular endothelial cells (CMECs), thereby alleviating MI/RI. Methods: A cardiac endothelium‑targeting peptide CRPPR was conjugated to DSPE‑PEG2000 to prepare a Sch‑loaded nanoparticle (CRPPR@Sch). MI/RI was induced in mice by 45‑minute ischemia followed by 6‑hour reperfusion. CRPPR@Sch, free Sch, or non‑targeted DSP@Sch was administered intravenously for seven consecutive days. Cardiac function, infarct size, microvascular integrity and ferroptosis‑related markers were evaluated in vivo. In vitro, CMECs were exposed to hypoxia/reoxygenation (H/R), and ferroptosis was assessed. Results: CRPPR@Sch efficiently accumulated in cardiac endothelial cells, improved cardiac function, reduced infarct size, restored microvascular perfusion, and alleviated CMEC injury. RNA‑seq indicated that CRPPR@Sch suppressed ferroptosis‑related pathways. In vitro and in vivo experiments demonstrated that CRPPR@Sch significantly up‑regulated GPX4 expression, reduced ROS, lipid peroxidation and ferroptosis markers. Moreover, TRIM25 expression was elevated in MI/RI mice and H/R‑injured CMECs. Co‑immunoprecipitation and molecular dynamics simulations revealed that Sch binds to GPX4 and interferes with TRIM25‑mediated GPX4 ubiquitination and degradation. Conclusion: CRPPR@Sch effectively delivers Sch to cardiac endothelium, stabilizes GPX4 by disrupting the TRIM25‑GPX4 interaction, and thus inhibits ferroptosis in CMECs, ultimately protecting against myocardial microvascular injury in MI/RI.
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