Evidence map›Paper›PMID 42267188›Full record

ArticleInternational journal of endocrinology2026

TRIM27 Ubiquitinates and Degrades PPARγ to Promote Osteogenic Differentiation of BMSCs and Alleviate Osteoporosis.

Liya Zhang, Junfeng Li, Benjuan Wu

Abstract read
In one paragraph

Article in International journal of endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

3 authors.

Liya ZhangDepartment of General Medicine, Tianjin First Central Hospital, Tianjin, 300192, China, tj-fch.com.
Junfeng LiDepartment of General Medicine, Tianjin First Central Hospital, Tianjin, 300192, China, tj-fch.com.ORCID https://orcid.org/0009-0003-1612-637X
Benjuan WuDepartment of Rheumatology and Immunology, Tianjin First Central Hospital, Tianjin, 300192, China, tj-fch.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: This study elucidates the role of TRIM27 in osteogenic differentiation and osteoporosis pathogenesis, focusing on its regulatory mechanism through PPARγ. Methods: TRIM27 expression was assessed during osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) via RT-qPCR and western blot. TRIM27 was knocked down (sh-TRIM27) or overexpressed (Lv-TRIM27) to evaluate its impact on alkaline phosphatase (ALP) activity, mineralization (Alizarin Red S staining), and osteogenic markers (COL1A1, OPN, and OCN). An ovariectomized (OVX) mouse osteoporosis model was established to analyze TRIM27 expression and bone microstructure (H&E staining). Co-immunoprecipitation (Co-IP) and cycloheximide chase assays identified TRIM27-PPARγ interactions and degradation dynamics. Rescue experiments combined sh-TRIM27 with PPARγ knockdown (sh-PPARγ) or the agonist rosiglitazone (ROZ). Results: TRIM27 expression increased 2.1-fold during BMSC osteogenic differentiation but decreased in OVX mice ( Conclusion: TRIM27, as a key osteogenic promoter, ameliorates osteoporosis by targeting the degradation of PPARγ. Our research reveals the potential of TRIM27 in treating bone metabolism disorders and may become a potential target for the treatment of osteoporosis.

Indexed as

BMSCsosteoporosisPPARγTRIM27

Identifiers

PMID42267188
PMCPMC13244134

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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.