Vascular dysfunction in Hutchinson-Gilford progeria syndrome

Yaping Zhao; Li Wang; Suowen Xu

doi:10.1016/j.molmed.2024.12.008

Vascular dysfunction in Hutchinson-Gilford progeria syndrome

Trends Mol Med. 2024 Dec 30:S1471-4914(24)00341-1. doi: 10.1016/j.molmed.2024.12.008. Online ahead of print.

Authors

Yaping Zhao¹, Li Wang², Suowen Xu³

Affiliations

¹ Department of Endocrinology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, China; Department of Biomedical Sciences, City University of Hong Kong, Hong Kong, China.
² Department of Biomedical Sciences, City University of Hong Kong, Hong Kong, China.
³ Department of Endocrinology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, China; Anhui Provincial Key Laboratory of Metabolic Health and Panvascular Diseases, Hefei, 23001, China. Electronic address: sxu1984@ustc.edu.cn.

PMID: 39741011
DOI: 10.1016/j.molmed.2024.12.008

Abstract

Most patients with Hutchinson-Gilford progeria syndrome (HGPS) succumb to cardiovascular disease. Recent studies by Barettino et al., Cardoso et al., and Vakili et al. utilized progeria mouse models to elucidate novel mechanisms by which vascular smooth muscle cell (VSMC) and endothelial cell (EC) dysfunction accelerate the progress of the disease, thus providing directions for the development of new targeted pharmaco-therapies.