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RESEARCH PAPER / 2025-07-31

Nicotinamide Mononucleotide Alleviates Aging Defects in Hutchinson-Gilford Progeria Syndrome.

Yuyan Xu, Mengchen Wu, Yuhang Fan, Jia Zhang, Dixuan Xue, Ming Zhang, Rouyi Shao, Limeng Cai, Xufeng Liao, Ling Zhang, Jin Zhang

Bone Marrow Transplantation Center of the First Affiliated Hospital, and Center for Stem Cell and Regenerative Medicine, Department of Basic Medical Sciences, and Liangzhu Laboratory, Zhejiang University School of Medicine, Hangzhou, China.Bone Marrow Transplantation Center of the First Affiliated Hospital, and Center for Stem Cell and Regenerative Medicine, Department of Basic Medical Sciences, and Liangzhu Laboratory, Zhejiang University School of Medicine, Hangzhou, China. · pubmed

Abstract

Hutchinson-Gilford progeria syndrome (HGPS) is a rare genetic disorder caused by mutations in the LMNA gene, leading to progerin accumulation and accelerated aging. Current therapeutic interventions remain limited. Here, we demonstrate that supplementation with nicotinamide mononucleotide (NMN) markedly ameliorates HGPS-associated phenotypes at both the cellular and organismal levels. In patient-derived induced pluripotent stem cell-mesenchymal stem cells, NMN supplementation enhanced NAD

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Research summary

Nicotinamide mononucleotide supplementation improves aging-related defects in Hutchinson-Gilford progeria syndrome. This research addresses a specific genetic cause of accelerated aging and explores a potential therapeutic intervention that could have broader implications for understanding and treating aging processes.

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