Nanodelivery of Brucine in Myocardial Ischemia-Reperfusion Injury: Mitochondrial PANoptosis, Cardiotoxicity, and Translational Barriers

Scritto il 26/10/2026
da Yi Guo

Int J Nanomedicine. 2026 Oct 21;21:616055. doi: 10.2147/IJN.S616055. eCollection 2026.

ABSTRACT

Myocardial ischemia-reperfusion injury remains a major unresolved component of infarct expansion after timely restoration of coronary blood flow. Brucine, a toxic alkaloid from Strychnos nux-vomica L. is an instructive but experimentally constrained case study because low-exposure cardioprotective signals coexist with cardiac ion-channel liability and uncertain clinical dosing. This Review evaluates whether nanodelivery could widen the therapeutic window of brucine by reducing circulating free drug, enriching exposure near injured myocardium and enabling mechanistic testing of mitochondrial quality control, regulated cell death and antioxidant repair. The evidence base is mapped across direct brucine cardiovascular studies, direct brucine toxicology, brucine formulation studies outside cardiac reperfusion, non-brucine cardiac nanomedicine and general material-design principles. We emphasize that brucine-loaded nanomedicine has not yet been validated as a therapy for myocardial ischemia-reperfusion injury; progress will require direct formulation-specific pharmacokinetics, myocardial biodistribution, hERG/QT safety, arrhythmia monitoring, large-animal efficacy and manufacturing-quality evidence.

PMID:42928913 | PMC:PMC13695940 | DOI:10.2147/IJN.S616055