Evidence map›Paper›PMID 33537834›Full record

ArticleMolecular medicine reports2021

Critical implication of the PTEN/PI3K/AKT pathway during BMP2-induced heterotopic ossification.

Jun Dong, Xiqiang Xu, Qingyu Zhang, Zenong Yuan, Bingyi Tan

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

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  15. MicroRNA-loaded biomaterials for osteogenesis.Frontiers in bioengineering and biotechnology · 2022
    Review
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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

5 authors at 2 institutions in 1 country.

Jun DongDepartment of Orthopaedics, Shandong Provincial Hospital, Affiliated to Shandong First Medical University, Jinan, Shandong 250021, P.R. China.
Xiqiang XuDepartment of Orthopaedics, Shandong Provincial Hospital, Affiliated to Shandong First Medical University, Jinan, Shandong 250021, P.R. China.
Qingyu ZhangDepartment of Orthopaedics, Shandong Provincial Hospital, Affiliated to Shandong First Medical University, Jinan, Shandong 250021, P.R. China.
Zenong YuanDepartment of Orthopaedics, Shandong Provincial Hospital, Affiliated to Shandong First Medical University, Jinan, Shandong 250021, P.R. China.
Bingyi TanDepartment of Orthopaedics, Shandong Provincial Hospital, Affiliated to Shandong First Medical University, Jinan, Shandong 250021, P.R. China.
Shandong First Medical University · CNShandong Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heterotopic ossification (HO) is characterized by extraskeletal ossification in soft tissue. Thus far, there is a lack of effective drug therapy against HO. Loss of PTEN in osteoblasts has been reported to accumulate bone mass in skeletal development and promote fracture healing in association with the activation of the PI3K/AKT pathway. However, the role of the PTEN/PI3K/AKT signaling in HO pathogenesis remains unknown. The present study investigated the implication of this pathway during BMP2‑induced osteogenic differentiation and ectopic bone formation. It was shown that overexpression of PTEN inhibited proliferation but stimulated apoptosis in mesenchymal pluripotent C3H10T1/2 cells. PTEN also inhibited BMP2‑induced osteoblast differentiation, whereas BMP2 repressed PTEN expression and subsequently activated PI3K/AKT. The PI3K inhibitor, LY294002, blocked BMP2‑induced osteoblastogenesis, suggesting that the PI3K/AKT pathway is critically required for BMP2 to initiate osteoblastogenesis. In vivo, implantation of BMP2 in muscle induced ectopic endochondral ossification. Strikingly, this bone‑forming capacity was notably suppressed by the PI3K inhibitor LY294002. Hence, the results of the present study demonstrated that the PI3K/AKT signaling activity is indispensable for BMP2 to induce ectopic new bone. Targeting the PI3K/AKT pathway using inhibitor(s) may represent a potential molecular therapy for the treatment against HO.

Indexed as

Signal TransductionAnimalsBone Morphogenetic Protein 2Cell LineMaleMiceMice, Inbred BALB COssification, HeterotopicPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseBmp2 protein, mouseBone Morphogenetic Protein 2Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePten protein, mouseheterotopic ossificationosteoblast differentiationPI3K/AKTPTEN

Identifiers

PMID33537834
PMCPMC7893754
OpenAlexW3129145672

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.