Trans-Organ Early Intervention for Myocardial Infarction Based on Bone Marrow-Homing Biomimetic Nanomedicine

Myocardial infarction (MI) elicits a robust inflammatory cascade, necessitating immunomodulatory strategies to attenuate neutrophil infiltration. Traditional invasive therapies, such as direct intramyocardial injections of anti-inflammatory factors or catheter-based local delivery of stem cells, are constrained by narrow therapeutic windows and can cause local tissue irritation and myocardial injury due to mechanical manipulation or puncture. Moreover, intravenous administration of anti-inflammatory agents often lacks specificity and targeted efficacy. Leveraging myeloma cell membrane-coated biomimetic nanomedicine encapsulating neutrophil chemotaxis inhibitors (MMNP@SB225002), a targeted therapeutic paradigm is engineered for the trans-organ early intervention modulation of the inflammatory cascade post-MI. By harnessing the bone marrow-homing (BMH) propensity, the therapeutic agent is efficiently trafficked to the bone marrow during the early post-MI response, markedly suppressing neutrophil mobilization. This strategy efficiently directs therapeutic agents to the bone marrow early after MI, significantly reducing neutrophil mobilization. By avoiding direct intervention at the infarction site and employing indirect modulation through peripheral immune organs, this approach sustainably mitigates myocardial fibrosis. The findings demonstrate that MMNP@SB225002 confers robust cardioprotection by alleviating post-MI inflammation. This innovative approach delineates a promising remote therapeutic strategy with substantial translational potential, underpinned by its enhanced safety profile.

biomimetic nanomedicine; bone marrow‐homing; myocardial infarction; neutrophils.