Evidence map›Paper›PMID 39011677›Full record

ArticleJournal of Zhejiang University. Science. B2024

Human umbilical cord mesenchymal stem cells attenuate diabetic nephropathy through the IGF1R-CHK2-p53 signalling axis in male rats with type 2 diabetes mellitus.

Hao Zhang, Xinshu Wang, Bo Hu, Peicheng Li, Yierfan Abuduaini, Hongmei Zhao, Ayinaer Jieensihan, Xishuang Chen, Shiyu Wang, Nuojin Guo and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of Zhejiang University. Science. B, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

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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

17 authors.

Hao ZhangDepartment of Endocrinology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China.
Xinshu WangResearch Center for Translational Medicine, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China.
Bo HuDepartment of Cardiology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China.
Peicheng LiDepartment of Endocrinology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China.
Yierfan AbuduainiDepartment of Endocrinology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China.
Hongmei ZhaoDepartment of Endocrinology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China.
Ayinaer JieensihanDepartment of Endocrinology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China.
Xishuang ChenDepartment of Endocrinology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China.
Shiyu WangDepartment of Endocrinology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China.
Nuojin GuoDepartment of Endocrinology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China.
Jian YuanResearch Center for Translational Medicine, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China.
Yunhui LiResearch Center for Translational Medicine, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China.
Lei LiResearch Center for Translational Medicine, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China.
Yuntong YangDepartment of Biochemistry and Molecular Biology, School of Medicine, Tongji University, Shanghai 200331, China.
Zhongmin LiuDepartment of Cardiology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China.
Zhaosheng TangDepartment of Endocrinology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China. tjwh02@163.com, zhaoshengtang@aliyun.com.
Hua WangDepartment of Endocrinology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200120, China. tjwh02@163.com.

Funding

the Natural Science Foundation of Jiangxi Province 20181ACB20021 and 20181BAB205044the Peak Disciplines (Type IV) of Institutions of Higher Learning in Shanghai, the Discipline Leader Program of Pudong New District Health and Family Planning Commission PWRd2018-02
6 · The paper itself

Abstract

Diabetes mellitus (DM) is a disease syndrome characterized by chronic hyperglycaemia. A long-term high-glucose environment leads to reactive oxygen species (ROS) production and nuclear DNA damage. Human umbilical cord mesenchymal stem cell (HUcMSC) infusion induces significant antidiabetic effects in type 2 diabetes mellitus (T2DM) rats. Insulin-like growth factor 1 (IGF1) receptor (IGF1R) is important in promoting glucose metabolism in diabetes; however, the mechanism by which HUcMSC can treat diabetes through IGF1R and DNA damage repair remains unclear. In this study, a DM rat model was induced with high-fat diet feeding and streptozotocin (STZ) administration and rats were infused four times with HUcMSC. Blood glucose, interleukin-6 (IL-6), IL-10, glomerular basement membrane, and renal function were examined. Proteins that interacted with IGF1R were determined through coimmunoprecipitation assays. The expression of IGF1R, phosphorylated checkpoint kinase 2 (p-CHK2), and phosphorylated protein 53 (p-p53) was examined using immunohistochemistry (IHC) and western blot analysis. Enzyme-linked immunosorbent assay (ELISA) was used to determine the serum levels of 8-hydroxydeoxyguanosine (8-OHdG). Flow cytometry experiments were used to detect the surface markers of HUcMSC. The identification of the morphology and phenotype of HUcMSC was performed by way of oil red "O" staining and Alizarin red staining. DM rats exhibited abnormal blood glucose and IL-6/10 levels and renal function changes in the glomerular basement membrane, increased the expression of IGF1 and IGF1R. IGF1R interacted with CHK2, and the expression of p-CHK2 was significantly decreased in

Indexed as

Checkpoint Kinase 2Diabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Diabetic NephropathiesMesenchymal Stem CellsMesenchymal Stem Cell TransplantationRats, Sprague-DawleyReceptor, IGF Type 1Signal TransductionTumor Suppressor Protein p53Umbilical CordAnimalsBlood GlucoseDiet, High-FatDNA DamageHumansBlood GlucoseCheckpoint Kinase 2IGF1R protein, humanIgf1r protein, ratReceptor, IGF Type 1Tumor Suppressor Protein p53Checkpoint kinase 2 (CHK2)Diabetes mellitusDNA damage repairHuman umbilical cord mesenchymal stem cell (HUcMSC)Insulin-like growth factor 1 receptor (IGF1R)Protein 53 (p53)

Identifiers

PMID39011677
PMCPMC11254681

What OpenQuestion holds

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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.