Evidence map›Paper›PMID 38348888›Full record

ArticleCell proliferation2024

Metformin rejuvenates Nap1l2-impaired immunomodulation of bone marrow mesenchymal stem cells via metabolic reprogramming.

Fan Liu, Ruohui Han, Shaochen Nie, Yuxin Cao, Xinming Zhang, Feng Gao, Zhengyang Wang, Liangyu Xing, Zhaoguang Ouyang, Lei Sui and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-weighted citation impact, top 20% of its field
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

8 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Metformin and bone metabolism: unraveling their direct and indirect effects.Therapeutic advances in endocrinology and metabolism · 2025
    Review
  6. Article
  7. Article
  8. Review
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

15 authors at 3 institutions in 2 countries.

Fan LiuDepartment of Endodontics and Laboratory of Stem Cells Endocrine Immunology, Tianjin Medical University School of Stomatology, Tianjin, China.
Ruohui HanDepartment of Endodontics and Laboratory of Stem Cells Endocrine Immunology, Tianjin Medical University School of Stomatology, Tianjin, China.
Shaochen NieDepartment of Endodontics and Laboratory of Stem Cells Endocrine Immunology, Tianjin Medical University School of Stomatology, Tianjin, China.
Yuxin CaoDepartment of Endodontics and Laboratory of Stem Cells Endocrine Immunology, Tianjin Medical University School of Stomatology, Tianjin, China.
Xinming ZhangDepartment of Endodontics and Laboratory of Stem Cells Endocrine Immunology, Tianjin Medical University School of Stomatology, Tianjin, China.
Feng GaoDepartment of Endodontics and Laboratory of Stem Cells Endocrine Immunology, Tianjin Medical University School of Stomatology, Tianjin, China.
Zhengyang WangDepartment of Endodontics and Laboratory of Stem Cells Endocrine Immunology, Tianjin Medical University School of Stomatology, Tianjin, China.
Liangyu XingDepartment of Endodontics and Laboratory of Stem Cells Endocrine Immunology, Tianjin Medical University School of Stomatology, Tianjin, China.
Zhaoguang OuyangDepartment of Endodontics and Laboratory of Stem Cells Endocrine Immunology, Tianjin Medical University School of Stomatology, Tianjin, China.
Lei SuiDepartment of Prosthodontics, Tianjin Medical University School of Stomatology, Tianjin, China.ORCID https://orcid.org/0000-0003-3586-9999
Wenyi MiTianjin Institute of Immunology, The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, Tianjin Medical University General Hospital, Tianjin Medical University, Tianjin, China.
Xudong WuState Key Laboratory of Experimental Hematology, The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Department of Cell Biology, Tianjin Medical University, Tianjin, China.ORCID https://orcid.org/0000-0001-9594-479X
Lu SunDepartment of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, Michigan, USA.
Meilin HuDepartment of Endodontics and Laboratory of Stem Cells Endocrine Immunology, Tianjin Medical University School of Stomatology, Tianjin, China.
Dayong LiuDepartment of Endodontics and Laboratory of Stem Cells Endocrine Immunology, Tianjin Medical University School of Stomatology, Tianjin, China.ORCID https://orcid.org/0000-0001-8511-2658
Tianjin Medical University · CNTianjin Medical University General Hospital · CNUniversity of Michigan · US

Funding

Jinmen Medical Talents Project of Tianjin Health Commission TJSJMYXYC-D2-025National Natural Science Foundation of China 82071079
6 · The paper itself

Abstract

Ageing and cell senescence of mesenchymal stem cells (MSCs) limited their immunomodulation properties and therapeutic application. We previously reported that nucleosome assembly protein 1-like 2 (Nap1l2) contributes to MSCs senescence and osteogenic differentiation. Here, we sought to evaluate whether Nap1l2 impairs the immunomodulatory properties of MSCs and find a way to rescue the deficient properties. We demonstrated that metformin could rescue the impaired migration properties and T cell regulation properties of OE-Nap1l2 BMSCs. Moreover, metformin could improve the impaired therapeutic efficacy of OE-Nap1l2 BMSCs in the treatment of colitis and experimental autoimmune encephalomyelitis in mice. Mechanistically, metformin was capable of upregulating the activation of AMPK, synthesis of l-arginine and expression of inducible nitric oxide synthase in OE-Nap1l2 BMSCs, leading to an increasing level of nitric oxide. This study indicated that Nap1l2 negatively regulated the immunomodulatory properties of BMSCs and that the impaired functions could be rescued by metformin pretreatment via metabolic reprogramming. This strategy might serve as a practical therapeutic option to rescue impaired MSCs functions for further application.

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalImmunomodulationMesenchymal Stem CellsMetforminMice, Inbred C57BLAnimalsBone Marrow CellsCell DifferentiationCell MovementCells, CulturedCellular ReprogrammingCellular SenescenceColitisMetabolic ReprogrammingMiceNitric OxideMetforminNitric OxideNitric Oxide Synthase Type II

Identifiers

PMID38348888
PMCPMC11216924
OpenAlexW4391785918

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.