Key result
Orally administered αCT11-loaded milk-derived extracellular vesicles reduced infarct size by >60% and preserved heart function in a mouse model of ischemia-reperfusion injury.
Why the study?
Extracellular vesicles hold promise for targeted drug delivery, but their therapeutic potential is limited by challenges in administration route, loading, targeted delivery, and production at scale.
Does orally administered αCT11-loaded milk-derived extracellular vesicles reduce infarct size and preserve heart function in a mouse model of ischemia-reperfusion injury?
Does orally administered αCT11-loaded milk-derived extracellular vesicles reduce infarct size and preserve heart function in a mouse model of ischemia-reperfusion injury?
Effect estimate: >60% reduction
Orally delivered milk-derived nanovesicles loaded with Cx43 peptides significantly reduce infarct size and preserve heart function in a preclinical mouse model of ischemia-reperfusion injury.
Extracellular vesicles have emerged as promising nanocarriers for targeted drug delivery, but their therapeutic potential is limited by challenges related to administration route, loading, targeted delivery and production at scale. Here, we report an innovative approach for targeted delivery of therapeutic peptides to injured tissues using milk-derived small extracellular vesicles (mEVs) as an abundant, safe, orally administrable nanoplatform. We demonstrate that a sub-population of mEVs naturally contain Connexin 43 (Cx43) and its Carboxyl-Terminal (CT) polypeptides, which have been shown to play crucial roles in wound healing and tissue repair. Leveraging this intrinsic property, we developed an esterification method to efficiently and uniformly load mEVs with enhanced levels of an exogenous Cx43 CT peptide (αCT11 - RPRPDDLEI), as assessed by flow cytometry-based vesicle quantification and mass spectrometry. These engineered mEVs exhibited remarkable injury targeting capabilities, with > 30-fold increases in uptake by injured cells compared to non-wounded cells in vitro and preferential accumulation in wounded tissues in vivo. Notably, αCT11-loaded mEVs orally administered after myocardial infarction reduced infarct size by >60% and preserved heart function in a mouse model of ischemia-reperfusion injury. This study represents a significant advance in nanomedicine, demonstrating the utilization of naturally occurring milk-derived extracellular vesicles as an oral delivery system for therapeutic peptides, achieving unprecedented targeting efficiency and efficacy in the treatment of myocardial ischemia-reperfusion injury.
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Marsh et al. (2025) studied Myocardial ischemia-reperfusion injury. αCT11-loaded milk-derived small extracellular vesicles (mEVs) was evaluated on Infarct size (>60% reduction). Orally administered αCT11-loaded milk-derived extracellular vesicles reduced infarct size by >60% and preserved heart function in a mouse model of ischemia-reperfusion injury.
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