Injured Myocardium-Targeted Theranostic Nanoplatform for Multi-Dimensional Immune-Inflammation Regulation in Acute Myocardial Infarction.

ABSTRACT: Pyroptosis is a key mode of programmed cell death during the early stages following acute myocardial infarction (AMI), driving immune-inflammatory responses. Cardiac resident macrophages (CRMs) are the primary mediators of cardiac immunity, and they serve a dual role through their shaping of both myocardial injury and post-AMI myocardial repair. To appropriately regulate AMI-associated inflammation, HM4oRL is herein designed, an innovative bifunctional therapeutic nanoplatform capable of inhibiting cardiomyocyte pyroptosis while reprogramming inflammatory signaling. This HM4oRL platform is composed of a core of 4-Octyl itaconate (4-OI)-loaded liposomes, a middle layer consisting of a metal-polyphenol network (MPN) film, and an optimized outer hybrid immune-cell membrane layer. The unique p

SUBMITTER: Zheng T 

PROVIDER: S-EPMC11904987 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature