Evidence map›Paper›PMID 40045380›Full record

ArticleStem cell research & therapy2025

Mesenchymal stem cell-derived small extracellular vesicles reduced hepatic lipid accumulation in MASLD by suppressing mitochondrial fission.

Yifei Chen, Fuji Yang, Yanjin Wang, Yujie Shi, Likang Liu, Wei Luo, Jing Zhou, Yongmin Yan

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Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

10 citing papers in PubMed.

  1. Article
  2. [Mesenchymal stem cell-derived exosomes: a new hope for metabolic-associated fatty liver disease].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Yifei Chen *Department of Laboratory Medicine, Wujin Hospital Affiliated with Jiangsu University, Changzhou, 213017, China.
Fuji Yang *Department of Laboratory Medicine, Wujin Hospital Affiliated with Jiangsu University, Changzhou, 213017, China.
Yanjin WangDepartment of Laboratory Medicine, Wujin Hospital Affiliated with Jiangsu University, Changzhou, 213017, China.
Yujie ShiDepartment of Laboratory Medicine, Wujin Hospital Affiliated with Jiangsu University, Changzhou, 213017, China.
Likang LiuDepartment of Laboratory Medicine, Wujin Hospital Affiliated with Jiangsu University, Changzhou, 213017, China.
Wei LuoWujin Institute of Molecular Diagnostics and Precision Cancer Medicine of Jiangsu University, Changzhou, 213017, China.
Jing ZhouWujin Institute of Molecular Diagnostics and Precision Cancer Medicine of Jiangsu University, Changzhou, 213017, China.
Yongmin YanDepartment of Laboratory Medicine, Wujin Hospital Affiliated with Jiangsu University, Changzhou, 213017, China. yym@wjrmyy.cn.ORCID http://orcid.org/0000-0002-1990-1170

Funding

Changzhou's 14th five-year plan project to train high-level health professionals 2022CZLJ027Changzhou Special Program for the Introduction of Foreign Talents CQ20240052National Natural Science Foundation of China 82272421Open project of Jiangsu Provincial Key Laboratory of Key Laboratory of Laboratory Medicine JSKLM-Z-2024-001
6 · The paper itself

Abstract

backgroundMetabolic dysfunction-associated steatotic liver disease (MASLD) is a chronic liver disease characterized by lipid accumulation in liver cells. Human umbilical cord mesenchymal stem cell-derived small extracellular vesicles (MSC-sEV) have great potential in repairing and regenerating liver diseases. However, it is still unclear whether MSC-sEV can inhibit hepatocyte lipid accumulation by regulating mitochondrial fission.

methodsWe investigated the effects of MSC-sEV on mitochondrial fission and its potential mechanism in lipotoxic hepatocytes and high-fat diet (HFD)-induced MASLD mice.

resultsWe found that MSC-sEV can effectively inhibit the expression of the Dynamin-related protein 1 (DRP1), thereby reducing mitochondrial fission, mitochondrial damage, and lipid deposition in lipotoxic hepatocytes and livers of HFD-induced MASLD in mice. Further mechanistic studies revealed that RING finger protein 31 (RNF31) played a crucial role in mediating the inhibitory effect of MSC-sEV on DRP1 and mitochondrial fission. RNF31 can suppress DRP1 expression and mitochondrial fission, thereby improving mitochondrial dysfunction and reducing hepatocyte lipid deposition. These findings suggest that MSC-sEV may downregulate hepatocyte DRP1-mediated mitochondrial fission by transporting RNF31, ultimately inhibiting hepatocyte lipid accumulation.

conclusionsThe insights from this study provide a new perspective on the mechanism of MSC-sEV in reducing lipid accumulation and offer a potential therapeutic target by targeting DRP1 to inhibit hepatocyte steatosis and the progression of MASLD.

Indexed as

Extracellular VesiclesFatty LiverLipid MetabolismMesenchymal Stem CellsMitochondrial DynamicsAnimalsDiet, High-FatDynaminsHepatocytesHumansLiverMaleMiceMice, Inbred C57BLUbiquitin-Protein LigasesDnm1l protein, mouseDynaminsUbiquitin-Protein LigasesDRP1MASLDMitochondrial fissionMSCSmall extracellular vesicles

Identifiers

PMID40045380
PMCPMC11884000

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.