Gelsolin's Protective Role in MASH through F‐Actin Regulation and P53 Degradation

Abstract Hepatic steatosis, inflammation, and fibrosis are the hallmarks of metabolic‐associated steatohepatitis (MASH), a serious health risk. This study emphasizes how important gelsolin (GSN) is to the pathophysiology of MASH. The results show that GSN is significantly overexpressed in both MASH...

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Main Authors: Yiwei Lu, Tong Ji, Zhichao Ye, Jianing Yan, Chao Wang, Jiachen Chen, Ziyang Jin, Yongji Zhu, Xiujun Cai, Yifan Wang
Format: Article
Language:English
Published: Wiley 2025-06-01
Series:Advanced Science
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Online Access:https://doi.org/10.1002/advs.202416489
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author Yiwei Lu
Tong Ji
Zhichao Ye
Jianing Yan
Chao Wang
Jiachen Chen
Ziyang Jin
Yongji Zhu
Xiujun Cai
Yifan Wang
author_facet Yiwei Lu
Tong Ji
Zhichao Ye
Jianing Yan
Chao Wang
Jiachen Chen
Ziyang Jin
Yongji Zhu
Xiujun Cai
Yifan Wang
author_sort Yiwei Lu
collection DOAJ
description Abstract Hepatic steatosis, inflammation, and fibrosis are the hallmarks of metabolic‐associated steatohepatitis (MASH), a serious health risk. This study emphasizes how important gelsolin (GSN) is to the pathophysiology of MASH. The results show that GSN is significantly overexpressed in both MASH patients and animal models. Under MASH models, Gsn knockout (KO) (Gsn−/−) mice demonstrate exacerbated hepatic steatosis, inflammation, and fibrosis, underscoring GSN's protective function. Remarkably, adeno‐associated virus (AAV)‐mediated restoration of Gsn substantially alleviates these pathological features, indicating its therapeutic potential. Mechanistically, the absence of GSN leads to increased F‐actin polymerization and heightened activation of Yes‐associated protein (YAP), thereby intensifying the inflammatory response. Subsequently, the experimental data identify a co‐expression relationship between GSN and MDM2, and GSN is found to facilitate the ubiquitination and subsequent degradation of P53 via MDM2, a crucial process for liver protection. These findings imply that GSN is essential for controlling important molecular pathways in MASH by encouraging P53's MDM2‐mediated degradation, which lessens the severity of hepatic steatosis. The research offers important new understandings of the molecular mechanisms of MASH and suggests GSN as a viable therapeutic target to reduce liver damage and preserve hepatic homeostasis.
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spelling doaj-art-324c794fe42543b4866571d1faa4e7902025-08-20T03:22:15ZengWileyAdvanced Science2198-38442025-06-011223n/an/a10.1002/advs.202416489Gelsolin's Protective Role in MASH through F‐Actin Regulation and P53 DegradationYiwei Lu0Tong Ji1Zhichao Ye2Jianing Yan3Chao Wang4Jiachen Chen5Ziyang Jin6Yongji Zhu7Xiujun Cai8Yifan Wang9Department of General Surgery Sir Run Run Shaw Hospital Affiliated to School of Medicine Zhejiang University Hangzhou 310016 ChinaDepartment of General Surgery Sir Run Run Shaw Hospital Affiliated to School of Medicine Zhejiang University Hangzhou 310016 ChinaDepartment of General Surgery Sir Run Run Shaw Hospital Affiliated to School of Medicine Zhejiang University Hangzhou 310016 ChinaDepartment of General Surgery Sir Run Run Shaw Hospital Affiliated to School of Medicine Zhejiang University Hangzhou 310016 ChinaDepartment of General Surgery Sir Run Run Shaw Hospital Affiliated to School of Medicine Zhejiang University Hangzhou 310016 ChinaDepartment of General Surgery Sir Run Run Shaw Hospital Affiliated to School of Medicine Zhejiang University Hangzhou 310016 ChinaDepartment of General Surgery Sir Run Run Shaw Hospital Affiliated to School of Medicine Zhejiang University Hangzhou 310016 ChinaDepartment of General Surgery Sir Run Run Shaw Hospital Affiliated to School of Medicine Zhejiang University Hangzhou 310016 ChinaDepartment of General Surgery Sir Run Run Shaw Hospital Affiliated to School of Medicine Zhejiang University Hangzhou 310016 ChinaDepartment of General Surgery Sir Run Run Shaw Hospital Affiliated to School of Medicine Zhejiang University Hangzhou 310016 ChinaAbstract Hepatic steatosis, inflammation, and fibrosis are the hallmarks of metabolic‐associated steatohepatitis (MASH), a serious health risk. This study emphasizes how important gelsolin (GSN) is to the pathophysiology of MASH. The results show that GSN is significantly overexpressed in both MASH patients and animal models. Under MASH models, Gsn knockout (KO) (Gsn−/−) mice demonstrate exacerbated hepatic steatosis, inflammation, and fibrosis, underscoring GSN's protective function. Remarkably, adeno‐associated virus (AAV)‐mediated restoration of Gsn substantially alleviates these pathological features, indicating its therapeutic potential. Mechanistically, the absence of GSN leads to increased F‐actin polymerization and heightened activation of Yes‐associated protein (YAP), thereby intensifying the inflammatory response. Subsequently, the experimental data identify a co‐expression relationship between GSN and MDM2, and GSN is found to facilitate the ubiquitination and subsequent degradation of P53 via MDM2, a crucial process for liver protection. These findings imply that GSN is essential for controlling important molecular pathways in MASH by encouraging P53's MDM2‐mediated degradation, which lessens the severity of hepatic steatosis. The research offers important new understandings of the molecular mechanisms of MASH and suggests GSN as a viable therapeutic target to reduce liver damage and preserve hepatic homeostasis.https://doi.org/10.1002/advs.202416489F‐actingelsolin (GSN)metabolic‐associated steatohepatitis (MASH)P53YAP
spellingShingle Yiwei Lu
Tong Ji
Zhichao Ye
Jianing Yan
Chao Wang
Jiachen Chen
Ziyang Jin
Yongji Zhu
Xiujun Cai
Yifan Wang
Gelsolin's Protective Role in MASH through F‐Actin Regulation and P53 Degradation
Advanced Science
F‐actin
gelsolin (GSN)
metabolic‐associated steatohepatitis (MASH)
P53
YAP
title Gelsolin's Protective Role in MASH through F‐Actin Regulation and P53 Degradation
title_full Gelsolin's Protective Role in MASH through F‐Actin Regulation and P53 Degradation
title_fullStr Gelsolin's Protective Role in MASH through F‐Actin Regulation and P53 Degradation
title_full_unstemmed Gelsolin's Protective Role in MASH through F‐Actin Regulation and P53 Degradation
title_short Gelsolin's Protective Role in MASH through F‐Actin Regulation and P53 Degradation
title_sort gelsolin s protective role in mash through f actin regulation and p53 degradation
topic F‐actin
gelsolin (GSN)
metabolic‐associated steatohepatitis (MASH)
P53
YAP
url https://doi.org/10.1002/advs.202416489
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