Targeted NAD⁺ repletion via biomimetic nanoparticle enables simultaneous management of intimal hyperplasia and accelerated re-endothelialization: A proof-of-concept study toward next-generation of endothelium-protective, anti-restenotic therapy.

ABSTRACT: Endovascular interventions often fail due to restenosis, primarily caused by smooth muscle cell (SMC) proliferation, leading to intimal hyperplasia (IH). Current strategies to prevent restenosis are far from perfect and impose significant collateral damage on the fragile endothelial cell (EC), causing profound thrombotic risks. Nicotinamide adenine dinucleotide (NAD⁺) is a co-enzyme and signaling substrate implicated in redox and metabolic homeostasis, with a pleiotropic role in protecting against cardiovascular diseases. However, a functional link between NAD⁺ repletion and the delicate duo of IH and EC regeneration has yet to be established. NAD⁺ repletion has been historically challenging due to its poor cellular uptake and low bioavailability. We have r

SUBMITTER: Yin L 

PROVIDER: S-EPMC11611612 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature