Authors
Xuting Li, Yi Yuan, Changhong Lian, Dongdong Zhu, Yan Wang, Zhenlei Jia
Published in
Journal of biomaterials applications. Pages 8853282261476791. Aug 12, 2026. Epub Aug 12, 2026.
Abstract
Atherosclerosis progression is closely linked to metabolic dysfunction of plaque macrophages, where inducible nitric oxide synthase (iNOS)-mediated pathological nitric oxide (NO) burst is a key driver of inflammation and oxidative stress. This study designed macrophage membrane-camouflaged liposomes (M-AN@Lip) for the co-delivery of nicotinamide mononucleotide (NMN) and L-arginine (L-Arg), aiming to precisely regulate macrophage NO metabolic homeostasis. In vitro experiments demonstrated that M-AN@Lip effectively increased intracellular NO generation while significantly downregulating the expression of the oxidative stress-related enzyme NAD(P)H quinone oxidoreductase 1 (NQO1), suggesting a reprogramming of macrophage NO metabolism from a pathological iNOS-dominated pathway towards a protective one. This metabolic shift was accompanied by clearance of intracellular reactive oxygen species (ROS), enhancement of the endogenous antioxidant enzyme system, and polarization of macrophages towards an anti-inflammatory M2 phenotype. Ultimately, M-AN@Lip significantly inhibited oxidized low-density lipoprotein (ox-LDL) uptake and foam cell formation by downregulating the expression of scavenger receptors (CD36, MSR1, SRB1). This study demonstrates that a biomimetic nano-system can achieve integrated anti-inflammatory, antioxidant, and anti-foam cell forming effects through the synergistic regulation of NO metabolism, offering a promising novel nanotherapeutic strategy for atherosclerosis.
PMID:
42581695
Bibliographic data and abstract were imported from PubMed on 12 Aug 2026.
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