Peptide-functionalized periodic mesoporous silica nanoparticles for monocyte-specific TET3 Silencing enhance cardiac repair after acute myocardial infarction.

ABSTRACT: Modulating the balance between pro- and anti-inflammatory monocyte subsets holds therapeutic promise in acute myocardial infarction (AMI); however, effective and selective strategies are still lacking. In this study, we are the first to identify Ten-Eleven-Translocation 3 (TET3) expression in circulating monocytes as an independent predictor of AMI occurrence and patient prognosis in a clinical cohort. Building on this novel insight, we engineered a monocyte-targeted RNAi delivery system designed to silence TET3 expression selectively. The platform employs periodic mesoporous silica nanoparticles (PMS) loaded with siTET3, and is surface-modified with polyethylenimine (PEI) and polyethylene glycol (PEG) to enhance cellular uptake. Critically, we further functionalized the system with a CD14

SUBMITTER: Jin H 

PROVIDER: S-EPMC12659391 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature