Evidence mapPaperPMID 42325620Full record

ArticleFrontiers in endocrinology2026

Metformin attenuates diabetic osteoporosis via the miR-21 mediated Mef2c/Sost pathway.

Le Liu, Jie Xu, Hui Zheng, Xiao-Chen Li, Zhong-Ai Gao, Cheng Meng, Congqing Pan, Ju-Hong Yang, Bao-Cheng Chang

Abstract read
In one paragraph

Article in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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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

9 authors.

Le Liu *Department of Geriatrics, Second Hospital of Tianjin Medical University, Tianjin, China.
Jie Xu *NHC Key Lab of Hormones and Development and Tianjin Key Lab of Metabolic Diseases, Tianjin Medical University Chu Hsien-I Memorial Hospital & Institute of Endocrinology, Tianjin, China.
Hui Zheng *Endocrinology Department, TEDA International Cardiovascular Hospital, Tianjin, China.
Xiao-Chen LiNHC Key Lab of Hormones and Development and Tianjin Key Lab of Metabolic Diseases, Tianjin Medical University Chu Hsien-I Memorial Hospital & Institute of Endocrinology, Tianjin, China.
Zhong-Ai GaoNHC Key Lab of Hormones and Development and Tianjin Key Lab of Metabolic Diseases, Tianjin Medical University Chu Hsien-I Memorial Hospital & Institute of Endocrinology, Tianjin, China.
Cheng MengDepartment of Nephrology, Kidney Disease Medical Center, General Hospital, Tianjin Medical University, National Key Clinical Specialty, Tianjin Key Medical Discipline, Tianjin, China.
Congqing PanNHC Key Lab of Hormones and Development and Tianjin Key Lab of Metabolic Diseases, Tianjin Medical University Chu Hsien-I Memorial Hospital & Institute of Endocrinology, Tianjin, China.
Ju-Hong YangGuangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Institute of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Bao-Cheng ChangNHC Key Lab of Hormones and Development and Tianjin Key Lab of Metabolic Diseases, Tianjin Medical University Chu Hsien-I Memorial Hospital & Institute of Endocrinology, Tianjin, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: ObjectiveThis study aimed to explore the role of the Methods: We compared bone mineral density (BMD), bone turnover biomarkers, and bone miR-21 expression levels between elderly female patients with and without diabetes. Diabetic mice and high-glucose-treated MLO-Y4 osteocytes were used to explore the involvement of the Results: Diabetic patients exhibited decreased bone miR-21 expression and reduced BMD, both of which were positively correlated with glycemic control status. Consistently, miR-21 was significantly downregulated in diabetic mice and high-glucose-cultured MLO-Y4 osteocytes. Both miR-21 and diabetic mice presented elevated protein levels of MEF2C and sclerostin, reduced expression of Cyclin D1 and RUNX2, as well as impaired bone strength and bone quality. As a direct target gene of miR-21, Conclusion: The

Indexed as

Adaptor Proteins, Signal TransducingDiabetes ComplicationsDiabetes Mellitus, ExperimentalMEF2 Transcription FactorsMetforminMicroRNAsOsteoporosisAgedAnimalsBone DensityFemaleGenetic MarkersHumansHypoglycemic AgentsMiceMice, Inbred C57BLAdaptor Proteins, Signal TransducingGenetic MarkersHypoglycemic AgentsMEF2C protein, humanMef2c protein, mouseMEF2 Transcription FactorsMetforminMicroRNAsMIRN21 microRNA, humanMIRN21 microRNA, mouseSost protein, mousediabetesmetforminmiR-21osteogenesisosteoporosissclerostin

Identifiers

PMID42325620
PMCPMC13278933

What Socratic holds

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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 Socratic graph.