FOXO4-DRI induces keloid senescent fibroblast apoptosis by promoting nuclear exclusion of upregulated p53-serine 15 phosphorylation

Abstract Keloids are pathological scars exhibiting tumour-like aggressiveness and high recurrence rate. Here we find increased proportion of pro-inflammatory and mesenchymal fibroblast subpopulations and senescent fibroblasts, and enhanced expression of senescence-associated secretory phenotype gene...

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Main Authors: Yu-Xiang Kong, Zhi-Shuai Li, Yuan-Bo Liu, Bo Pan, Xin Fu, Ran Xiao, Li Yan
Format: Article
Language:English
Published: Nature Portfolio 2025-02-01
Series:Communications Biology
Online Access:https://doi.org/10.1038/s42003-025-07738-0
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author Yu-Xiang Kong
Zhi-Shuai Li
Yuan-Bo Liu
Bo Pan
Xin Fu
Ran Xiao
Li Yan
author_facet Yu-Xiang Kong
Zhi-Shuai Li
Yuan-Bo Liu
Bo Pan
Xin Fu
Ran Xiao
Li Yan
author_sort Yu-Xiang Kong
collection DOAJ
description Abstract Keloids are pathological scars exhibiting tumour-like aggressiveness and high recurrence rate. Here we find increased proportion of pro-inflammatory and mesenchymal fibroblast subpopulations and senescent fibroblasts, and enhanced expression of senescence-associated secretory phenotype genes using single-cell RNA sequencing analysis, as well as elevated p16 protein and more β-galactosidase-positive cells in keloids. The up-regulated p53-serine15 phosphorylation (p53-pS15) in keloids is identified by phosphospecific protein microarray and western blotting. We further demonstrate that a senolytic FOXO4-D-retro-inverso-isoform peptide (FOXO4-DRI) promotes apoptosis and decreases G0/G1 phase cells in pro-senescence models of keloid organ cultures and fibroblasts, accompanied with p53-pS15 nuclear exclusion. Our study indicates that upregulation of p53-pS15 and p16 maintains a persistent senescent microenvironment to promote cell cycle arrest and apoptosis resistance in keloid fibroblasts. FOXO4-DRI shows potential as a treatment targeting the senescence and apoptosis resistance, and holds promise as an approach to prevent the aggressiveness and relapse of keloids.
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issn 2399-3642
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spelling doaj-art-001df97ec6f04bedace2897f00a3e90c2025-08-20T01:56:01ZengNature PortfolioCommunications Biology2399-36422025-02-018111310.1038/s42003-025-07738-0FOXO4-DRI induces keloid senescent fibroblast apoptosis by promoting nuclear exclusion of upregulated p53-serine 15 phosphorylationYu-Xiang Kong0Zhi-Shuai Li1Yuan-Bo Liu2Bo Pan3Xin Fu4Ran Xiao5Li Yan6Research Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical CollegeResearch Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical CollegeDepartment of Plastic and Reconstructive Surgery, Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical CollegeAuricular Plastic and Reconstructive Surgery Center, Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical CollegeResearch Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical CollegeResearch Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical CollegeResearch Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical CollegeAbstract Keloids are pathological scars exhibiting tumour-like aggressiveness and high recurrence rate. Here we find increased proportion of pro-inflammatory and mesenchymal fibroblast subpopulations and senescent fibroblasts, and enhanced expression of senescence-associated secretory phenotype genes using single-cell RNA sequencing analysis, as well as elevated p16 protein and more β-galactosidase-positive cells in keloids. The up-regulated p53-serine15 phosphorylation (p53-pS15) in keloids is identified by phosphospecific protein microarray and western blotting. We further demonstrate that a senolytic FOXO4-D-retro-inverso-isoform peptide (FOXO4-DRI) promotes apoptosis and decreases G0/G1 phase cells in pro-senescence models of keloid organ cultures and fibroblasts, accompanied with p53-pS15 nuclear exclusion. Our study indicates that upregulation of p53-pS15 and p16 maintains a persistent senescent microenvironment to promote cell cycle arrest and apoptosis resistance in keloid fibroblasts. FOXO4-DRI shows potential as a treatment targeting the senescence and apoptosis resistance, and holds promise as an approach to prevent the aggressiveness and relapse of keloids.https://doi.org/10.1038/s42003-025-07738-0
spellingShingle Yu-Xiang Kong
Zhi-Shuai Li
Yuan-Bo Liu
Bo Pan
Xin Fu
Ran Xiao
Li Yan
FOXO4-DRI induces keloid senescent fibroblast apoptosis by promoting nuclear exclusion of upregulated p53-serine 15 phosphorylation
Communications Biology
title FOXO4-DRI induces keloid senescent fibroblast apoptosis by promoting nuclear exclusion of upregulated p53-serine 15 phosphorylation
title_full FOXO4-DRI induces keloid senescent fibroblast apoptosis by promoting nuclear exclusion of upregulated p53-serine 15 phosphorylation
title_fullStr FOXO4-DRI induces keloid senescent fibroblast apoptosis by promoting nuclear exclusion of upregulated p53-serine 15 phosphorylation
title_full_unstemmed FOXO4-DRI induces keloid senescent fibroblast apoptosis by promoting nuclear exclusion of upregulated p53-serine 15 phosphorylation
title_short FOXO4-DRI induces keloid senescent fibroblast apoptosis by promoting nuclear exclusion of upregulated p53-serine 15 phosphorylation
title_sort foxo4 dri induces keloid senescent fibroblast apoptosis by promoting nuclear exclusion of upregulated p53 serine 15 phosphorylation
url https://doi.org/10.1038/s42003-025-07738-0
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