吡喃结构域
炎症体
神经科学
医学
细胞生物学
化学
受体
生物
内科学
作者
Damiano G. Barone,Alejandro Carnicer‐Lombarte,Panagiotis Tourlomousis,Russell S. Hamilton,Malwina Prater,Alexandra L. Rutz,Ivan B. Dimov,George G. Malliaras,Stéphanie P. Lacour,Avril A. B. Robertson,Kristian Franze,James W. Fawcett,Clare Bryant
标识
DOI:10.1073/pnas.2115857119
摘要
SignificanceImplantable electronic medical devices (IEMDs) are used for some clinical applications, representing an exciting prospect for the transformative treatment of intractable conditions such Parkinson's disease, deafness, and paralysis. The use of IEMDs is limited at the moment because, over time, a foreign body reaction (FBR) develops at the device-neural interface such that ultimately the IEMD fails and needs to be removed. Here, we show that macrophage nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activity drives the FBR in a nerve injury model yet integration of an NLRP3 inhibitor into the device prevents FBR while allowing full healing of damaged neural tissue to occur.
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