Mechanistic Study of Platelet Membrane-Coated Resveratrol Nanosystem in Mitochondrial Dysfunction and Endothelial Senescence During Atherosclerotic Lesion Development via FOXM1 Activation.
L, X., Z, Z., P, L., & B, Q. (2026). Mechanistic Study of Platelet Membrane-Coated Resveratrol Nanosystem in Mitochondrial Dysfunction and Endothelial Senescence During Atherosclerotic Lesion Development via FOXM1 Activation.. Aging cell. https://doi.org/10.1111/acel.70632
L X, Z Z, P L, B Q. Mechanistic Study of Platelet Membrane-Coated Resveratrol Nanosystem in Mitochondrial Dysfunction and Endothelial Senescence During Atherosclerotic Lesion Development via FOXM1 Activation.. Aging cell. 2026; doi: 10.1111/acel.70632
L X, Z Z, P L, et al. Mechanistic Study of Platelet Membrane-Coated Resveratrol Nanosystem in Mitochondrial Dysfunction and Endothelial Senescence During Atherosclerotic Lesion Development via FOXM1 Activation.[J]. Aging cell. 2026. DOI: 10.1111/acel.70632.
@article{l2026,
author = {Xiao L and Zhan Z and Liu P and Qin B},
title = {Mechanistic Study of Platelet Membrane-Coated Resveratrol Nanosystem in Mitochondrial Dysfunction and Endothelial Senescence During Atherosclerotic Lesion Development via FOXM1 Activation.},
journal = {Aging cell},
year = {2026},
doi = {10.1111/acel.70632},
note = {PMID: 42479952},
}
TY - JOUR AU - Xiao L AU - Zhan Z AU - Liu P AU - Qin B TI - Mechanistic Study of Platelet Membrane-Coated Resveratrol Nanosystem in Mitochondrial Dysfunction and Endothelial Senescence During Atherosclerotic Lesion Development via FOXM1 Activation. T2 - Aging cell PY - 2026 DO - 10.1111/acel.70632 AN - PMID:42479952 ER -
Atherosclerosis (AS) is closely linked to endothelial cell (EC) senescence and mitochondrial dysfunction, which impair vascular repair. Resveratrol (RSV) has antioxidant, anti-inflammatory, and pro-angiogenic effects, but its clinical use is restricted by poor bioavailability. This study aimed to construct a platelet membrane-coated resveratrol nanosystem (PM@RSV NPs) and investigate its mechanism of action in delaying the progression of AS by activating FOXM1 to improve mitochondrial function, inhibit EC senescence, and promote vascular regeneration. PM@RSV NPs were prepared using a solvent evaporation method combined with membrane-coating technology, and gene expression profiles and key regulatory networks were analyzed through RNA sequencing (RNA-seq), gene set enrichment analysis (GSEA), and least absolute shrinkage and selection operator (LASSO) regression. In vitro, PM@RSV NPs enhanced mitochondrial membrane potential and ATP generation while decreasing ROS accumulation and the number of SA-β-Gal-positive cells, accompanied by FOXM1 upregulation in ECs. In vivo experiments demonstrated that PM@RSV NPs significantly reduced plaque area, improved mitochondrial function, decreased levels of senescence markers, and promoted vascular regeneration via FOXM1 regulation. In addition, PM@RSV NPs preferentially accumulated in ox-LDL-injured MAECs and AS lesion-associated vascular endothelium, mainly through platelet-membrane adhesion proteins such as GPV and P-selectin; their biosafety was evaluated by EC viability/apoptosis assays, histological examination of major organs, and serum biochemical indices of liver and kidney function. This study confirmed that PM@RSV NPs improved mitochondrial function, inhibited endothelial senescence, and enhanced vascular regeneration by activating FOXM1, offering a novel therapeutic strategy for treating AS.