Evidence map›Paper›PMID 41844848›Full record

ArticleCell regeneration (London, England)2026

HUMSCs repair CCl₄-induced chronic liver injury in rats via metabolic regulation.

Changpeng Xie, Yiming Dong, Xinxin Yin, Jin Zeng, Zhanhai Su, Haiyan Wang, Jing Zhao, Qiong Wu, Panjian Wei, Ziyu Wang and 6 more

Abstract read
In one paragraph

Article in Cell regeneration (London, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

Changpeng Xie *Department of Basic Medical Sciences, Qinghai University Medical College, No.251 of Ningda Road, Xining, Qinghai, 810016, China.
Yiming Dong *Department of Oncology, Hebei General Hospital, No.348 Heping West Road, Xinhua District, Shijiazhuang, Hebei Province, 050051, China.
Xinxin Yin *Department of Basic Medical Sciences, Qinghai University Medical College, No.251 of Ningda Road, Xining, Qinghai, 810016, China.
Jin ZengDepartment of Basic Medical Sciences, Qinghai University Medical College, No.251 of Ningda Road, Xining, Qinghai, 810016, China.
Zhanhai SuDepartment of Basic Medical Sciences, Qinghai University Medical College, No.251 of Ningda Road, Xining, Qinghai, 810016, China.
Haiyan WangDepartment of Basic Medical Sciences, Qinghai University Medical College, No.251 of Ningda Road, Xining, Qinghai, 810016, China.
Jing ZhaoDepartment of Basic Medical Sciences, Qinghai University Medical College, No.251 of Ningda Road, Xining, Qinghai, 810016, China.
Qiong WuDepartment of Basic Medical Sciences, Qinghai University Medical College, No.251 of Ningda Road, Xining, Qinghai, 810016, China.
Panjian WeiCancer Research Center, Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, No.9 Beiguan Street, Tongzhou District, Beijing, 101149, China.
Ziyu WangCancer Research Center, Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, No.9 Beiguan Street, Tongzhou District, Beijing, 101149, China.
Meng GuCancer Research Center, Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, No.9 Beiguan Street, Tongzhou District, Beijing, 101149, China.
Xudong ZhangResearch Center of High Altitude Medicine, No.340 Qiyi Road, Chengzhong District, Xining, Qinghai Province, 810000, China.
Xianzong MaSenior Department of Gastroenterology, The First Medical Center of Chinese PLA General Hospital, Haidian District, Beijing, 100853, China. maxianzong@tmmu.edu.cn.
Yong DengQinghai Special Hospital of Cardio-Cerebrovascular Disease, No.7 Zhuanchang Road, Chengzhong District, Xining, Qinghai Province, 810000, China. 23259478@qq.com.
Yuanming PanCancer Research Center, Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, No.9 Beiguan Street, Tongzhou District, Beijing, 101149, China. peterfpan2020@mail.ccmu.edu.cn.
Juan AnDepartment of Basic Medical Sciences, Qinghai University Medical College, No.251 of Ningda Road, Xining, Qinghai, 810016, China. anjuan@qhu.edu.cn.ORCID http://orcid.org/0000-0002-0465-4867

Funding

Applied Basic Research Project of Science and Technology Department of Qinghai Province 2023-ZJ-754Beijing Municipal Administration of Hospital Incubating Program NO.PX2023059The National Natural Science Foundation of China 82260846
6 · The paper itself

Abstract

BACKGROUND AND

aimsTo explore the therapeutic effects of human umbilical cord mesenchymal stem cells (HUMSCs) on repairing CCl₄-induced chronic liver injury in rats via intravenous injection and to identify the associated key metabolites.

methodsCell experiments: THLE-2 cells were divided into blank control, CCl₄-treated, and CCl₄ + Exos groups. Cell viability was assessed using the CCK-8 assay, while levels of AST, ALT, and MDA were determined using commercial kits. Targeted metabolomics analysis was employed to identify differentially expressed metabolites. Transmission electron microscopy (TEM) was used to evaluate mitochondrial morphology, and immunofluorescence staining was performed to examine the colocalization of Exos with mitochondria. Animal experiments: 24 healthy SPF SD rats were randomly divided into healthy, CCl₄, and CCl₄ + HUMSCs groups (n = 8 per group). Serum samples were collected for biochemical detection and targeted metabolomics analyses, while liver tissues underwent histopathological examination. Immunofluorescence staining was employed to monitor HUMSCs enrichment.

resultsIn the CCl₄ + Exos group, cell viability was significantly restored, and the elevated levels of AST, ALT, and MDA were reversed, while mitochondrial ultrastructure was ameliorated with successful Exos-mitochondria colocalization. Targeted metabolomics confirmed the presence of differentially expressed metabolites exhibiting consistent trends in both cellular and animal models. In the animal study, the CCl₄ group showed significant liver dysfunction and hepatic pathology characterized by hepatocyte steatosis and fibrous tissue hyperplasia. In contrast, the CCl₄ + HUMSCs group demonstrated markedly improved liver function and reduced pathological changes. Biochemical analysis revealed significant differences in ALT, AST, ALB, TBIL, TP, UREA, CR, and UA levels between the CCl₄ + HUMSCs and CCl₄ groups. Serum metabolomics analysis showed that compared with the CCl₄ group, 1,7-Dimethylxanthine and Xanthosine were significantly upregulated, while Succinic Acid, (S)-2-Hydroxybutanoic Acid, oxidized glutathione, and 3'-Sialyllactose were significantly downregulated in the CCl₄ + HUMSCs group.

conclusionHUMSCs treatment significantly reduced hepatic steatosis and fibrosis compared with the CCl₄ group alone. Metabolomic analysis suggests that the underlying mechanisms may involve upregulation of propanoate metabolism and increased taurochenodeoxycholic acid levels, which warrant further investigation.

Indexed as

Carbon tetrachlorideChronic liver injuryMesenchymal stem cellMetabolitesSerum metabolomics

Identifiers

PMID41844848
PMCPMC12996463

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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.