Evidence map›Paper›PMID 41878315›Full record

ArticleAmerican journal of stem cells2026

GDF11 activates AMPK-dependent mitophagy to drive osteogenic differentiation of rat bone marrow mesenchymal stem cells.

Xinfeng Gao, Qiting He, Junjun Chen, Gen Wu, Shaoqiang Xia, Shuaiwei Shang, Linghang Xue, Xinqiang Bei, Kai Xiao

Abstract read
In one paragraph

Article in American journal of stem cells, 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

9 authors.

Xinfeng GaoDepartment of Orthopedic Surgery, Wuhan Fourth Hospital Wuhan 430030, Hubei, China.
Qiting HeDepartment of Orthopedic Surgery, Wuhan Fourth Hospital Wuhan 430030, Hubei, China.
Junjun ChenDepartment of Orthopedic Surgery, Wuhan Fourth Hospital Wuhan 430030, Hubei, China.
Gen WuDepartment of Orthopedic Surgery, Wuhan Fourth Hospital Wuhan 430030, Hubei, China.
Shaoqiang XiaDepartment of Orthopedic Surgery, Wuhan Fourth Hospital Wuhan 430030, Hubei, China.
Shuaiwei ShangDepartment of Orthopedic Surgery, Wuhan Fourth Hospital Wuhan 430030, Hubei, China.
Linghang XueDepartment of Orthopedic Surgery, Wuhan Fourth Hospital Wuhan 430030, Hubei, China.
Xinqiang BeiDepartment of Orthopedic Surgery, Wuhan Fourth Hospital Wuhan 430030, Hubei, China.
Kai XiaoDepartment of Orthopedic Surgery, Wuhan Fourth Hospital Wuhan 430030, Hubei, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGrowth differentiation factor 11 (GDF11) has emerged as a potential regulator of bone regeneration; however, the molecular mechanisms through which it influences osteogenic differentiation, particularly in relation to mitochondrial quality control, remain unclear. This study aimed to elucidate the role of adenosine monophosphate-activated protein kinase (AMPK)-dependent mitophagy in GDF11-mediated osteogenic differentiation of rat bone marrow mesenchymal stem cells (rBMMSCs).

methodsrBMMSCs were induced toward osteogenic differentiation with or without GDF11 treatment. To specifically inhibit AMPK-dependent mitophagy, Compound C, an AMPK inhibitor, was employed. Osteogenic differentiation was evaluated using alkaline phosphatase (ALP) staining and activity assays, while Alizarin Red S (ARS) staining was performed to assess matrix mineralization. The expression of Mitophagy- and osteogenesis-associated markers was analyzed through immunofluorescence staining, quantitative real-time PCR, and western blotting.

resultsGDF11 significantly enhanced the osteogenic differentiation of rBMMSCs, as evidenced by increased ALP activity, more intense ALP staining, enhanced calcium nodule formation, and elevated expression of ALP and RUNX2. GDF11 activated mitochondrial function by promoting AMPK phosphorylation and inducing Mitophagy. Inhibition of AMPK significantly impaired Mitophagy, while Compound C-mediated blockade of AMPK-dependent mitophagy not only suppressed basal osteogenic differentiation but also abolished the pro-osteogenic effects of GDF11. This was reflected by a pronounced reduction in GDF11-induced ALP activity, mineralization, and the expression of key osteogenic genes at both the mRNA and protein levels.

conclusionGDF11 enhances the osteogenic differentiation of rBMMSCs by activating AMPK-dependent mitophagy. These findings identify AMPK-dependent Mitophagy as a pivotal mechanism mediating the osteogenic actions of GDF11, providing new mechanistic insights that may guide the development of novel strategies for bone regeneration.

Indexed as

AMPKbone marrow mesenchymal stem cellsGrowth differentiation factor 11mitophagyosteogenic differentiation

Identifiers

PMID41878315
PMCPMC13006738

What OpenQuestion holds

Textmetadata
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.