Authors
Qipeng Wu, Yuan Xiong, Li Lu, Han Wang, Hui Hu, Mohammad-Ali Shahbazi, Guohui Liu, Bobin Mi
Published in
Advanced healthcare materials. Pages e71456. Jul 26, 2026. Epub Jul 26, 2026.
Abstract
Chronic diabetic wounds are characterized by persistent inflammation, impaired angiogenesis, and disrupted intercellular communication, including altered macrophage-endothelial interactions. In this study, we develop macrophage membrane-camouflaged, didymin (DM)-loaded metal-organic framework microneedles (Mac@DM-MOF MNs), a biomimetic nanozyme platform designed to selectively restore this intercellular communication and re-establish a pro-regenerative microenvironment. RNA-seq and mechanistic analyses identify activation of the SPP1-ApoE signaling axis, an unrecognized pathway linking M2 polarization to endothelial activation, as a central mechanism by which Mac@DM-MOF MNs synchronize inflammation resolution and angiogenesis. Nanozyme-mediated ROS scavenging relieves redox stress, while DM promotes macrophage polarizationtoward the reparative M2 state. M2-derived SPP1 subsequently interacts with endothelial ApoE, thereby promoting endothelial sprouting, and restoring vascular functionality. In diabetic mouse and Bama mini pig models, Mac@DM-MOF MNs attenuate inflammation, rescue angiogenic deficits, and markedly accelerate wound closure. Importantly, vascular restoration further reinforces M2 polarization, forming a self-sustaining pro-healing feedback loop. Our findings define macrophage-endothelial coupling as a pivotal regulatory mechanism in diabetic wound repair and introduce a synergistic nanomedicine-based strategy that concurrently resolves chronic inflammation and restores angiogenesis.
PMID:
42503243
Bibliographic data and abstract were imported from PubMed on 27 Jul 2026.
Read full publication at:
Please sign in
to see all details.
Advertisement
Stats
- Recommendations n/a n/a positive of 0 vote(s)
- Views 6
- Comments 0