Reprogramming monocytes into M2 macrophages as living drug depots to enhance treatment of myocardial ischemia-reperfusion injury

Delivering therapeutic agents efficiently to inflamed regions remains an intractable challenge following myocardial ischemia-reperfusion injury (MI/RI) due to the transient nature of the enhanced permeability and retention effect, which disappears after 24 h. Leveraging the inflammation-homing and p...

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Veröffentlicht in:	Journal of controlled release 2024-10, Vol.374, p.639-652
Hauptverfasser:	Liu, Yan, Zhou, Meiling, Xu, Maochang, Wang, Xueqin, Zhang, Yingying, Deng, Yiping, Zhang, Zongquan, Jiang, Jun, Zhou, Xiangyu, Li, Chunhong
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Anti-Inflammatory Agents - administration & dosage Anti-Inflammatory Agents - pharmacology Betamethasone - administration & dosage Betamethasone - analogs & derivatives Cellular Reprogramming - drug effects Drug Carriers - chemistry Ferrocyanides - chemistry Inflammation-homing Living drug depots M2 macrophages Macrophages - drug effects Male Mice Mice, Inbred C57BL Monocytes - drug effects Myocardial ischemia-reperfusion injury Myocardial Reperfusion Injury - drug therapy Nanoparticles - chemistry Reactive Oxygen Species - metabolism Reprogram
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