Evidence map›Paper›PMID 40402971›Full record

ArticlePLoS neglected tropical diseases2025

ADSCs attenuate Liver fibrosis via inducing HSC senescence: validation in dual-etiology models.

Mukexina Mulati, Ning Yang, Junlong Xue, Liang Li, Xue Zhang, Hui Liu, Jin Chu, Guodong Lü, Nuerbaiti Kusuman, Xiaolong He and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PLoS neglected tropical diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
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

13 authors.

Mukexina MulatiState Key Laboratory of Pathogenesis, Prevention, and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Ning YangState Key Laboratory of Pathogenesis, Prevention, and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Junlong XueState Key Laboratory of Pathogenesis, Prevention, and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Liang LiState Key Laboratory of Pathogenesis, Prevention, and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Xue ZhangState Key Laboratory of Pathogenesis, Prevention, and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Hui LiuState Key Laboratory of Pathogenesis, Prevention, and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Jin ChuState Key Laboratory of Pathogenesis, Prevention, and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Guodong LüState Key Laboratory of Pathogenesis, Prevention, and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Nuerbaiti KusumanState Key Laboratory of Pathogenesis, Prevention, and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Xiaolong HeState Key Laboratory of Pathogenesis, Prevention, and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Tuerganaili AjiDepartment of Hepatobiliary and Hydatid Diseases, Digestive and Vascular Surgery Center, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.ORCID 0000-0001-6737-8874
Xiaojuan BiState Key Laboratory of Pathogenesis, Prevention, and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Renyong LinState Key Laboratory of Pathogenesis, Prevention, and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.ORCID 0000-0001-6210-4719

Funding

Key Program of Xinjiang Natural Science FoundationNational Natural Science Foundation of ChinaState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central AsiaXinjiang Graduate Innovation ProgramXinjiang Natural Science FoundationXinjiang Regional Collaborative Innovation ProgramXinjiang Science Foundation for Distinguished Young ScholarsXinjiang Tianshan Project
6 · The paper itself

Abstract

backgroundLiver fibrosis (LF) results from various causes, which require finding conserved mechanisms to help treat related diseases. Although adipose-derived stem cells (ADSCs) transplantation can alleviate hepatic fibrosis, their mechanism remains unclear. Accordingly, we explored the efficacy and mechanisms behind ADSCs transplantation in two LF models. METHODOLOGY: The carbon tetrachloride (CCl4)-induced liver injury and Echinococcus multilocularis (E. multilocularis) infection models were established, and ADSCs were transplanted. Mouse liver samples were harvested and analyzed histologically. Expression levels of fibrosis and senescence-related proteins were analyzed by immunohistochemistry. Hepatic stellate cells (HSCs) activation and cell senescence protein expression were evaluated via western blotting. Co-localization expression was determined by immunofluorescence. To assess the cellular senescence degree, we utilized senescence-associated β-galactosidase (SA-β-Gal) staining.

resultIn the CCl4-induced LF mouse model, the liver surface exhibited a rough texture. The hematoxylin and eosin (H&E) staining revealed hepatic parenchymal cell destruction accompanied by pseudolobule formation and fibrosis in the portal area. In the E. multilocularis infection model, multiple white foci were on the liver surface. The H&E staining revealed massive inflammatory cell infiltration around the foci with severe fibrosis, and Sirius Red confirmed collagen deposition; both had elevated HSCs activation (α-SMA expression). After ADSCs transplantation, the collagen deposition and HSCs activation significantly diminished, while the cellular senescence levels increased. Immunofluorescence co-localization of p21 and a-SMA showed that transplantation of ADSCs promoted senescence of activated HSCs (aHSCs). In vitro co-culture had similar results, accompanied by expression changes and TGF-β/Smad signaling inhibition.

conclusionOur findings indicate that ADSCs transplantation can mitigate fibrosis by inducing the senescence of aHSCs and reducing collagen production.

Indexed as

Adipose TissueCellular SenescenceHepatic Stellate CellsLiver CirrhosisStem CellsStem Cell TransplantationAnimalsCarbon TetrachlorideDisease Models, AnimalLiverMaleMiceMice, Inbred C57BLCarbon Tetrachloride

Identifiers

PMID40402971
PMCPMC12148229

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.