Evidence map›Paper›PMID 39450541›Full record

ReviewInternational journal of molecular medicine2025

Role of NEL‑like molecule‑1 in osteogenesis/chondrogenesis (Review).

Zihan Li, Yihao Tian

Abstract readReview
In one paragraph

Review in International journal of molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. NELL-1: role and mechanisms in disease pathogenesis and development.Frontiers in cell and developmental biology · 2026
    Review
  3. m6A: a novel strategy for osteoporosis treatment.Frontiers in cell and developmental biology · 2025
    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

2 authors.

Zihan LiShengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Yihao TianDepartment of Pathology, Beifang Hospital of China Medical University, General Hospital of Northern Theater Command, Shenyang, Liaoning 110004, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A dynamic balance exists between osteogenesis and osteoclastogenesis in bone tissue, which can lead to several bone diseases, such as osteoporosis, osteoarthritis, bone necrosis and bone defects, in cases of insufficient osteogenesis or excessive osteoclastogenesis. NEL‑like molecule‑1 (NELL‑1) was first discovered in 1999 as an osteogenic factor that can prevent or treat bone diseases by increasing osteogenic levels. To date, research has identified multiple signaling pathways involved in improving osteogenic levels. Furthermore, to apply NELL‑1 in clinical practice, researchers have optimized its osteogenic effect by combining it with other molecules, changing its molecular structure and performing bone tissue engineering. Currently, research on NELL‑1 is gaining increasing attention. In the near future, it will definitely be applied in clinical practice to eliminate diseases. Thus, the present study provides a comprehensive review of NELL‑1 in enhancing osteogenic levels from the perspectives of the molecular mechanism, interactions with other molecules/cells, molecular‑level changes, applications in bone tissue engineering and its expression in tumors, providing a solid theoretical basis for its clinical application.

Indexed as

ChondrogenesisOsteogenesisAnimalsCalcium-Binding ProteinsHumansNerve Tissue ProteinsSignal TransductionTissue EngineeringCalcium-Binding ProteinsNELL1 protein, humanNerve Tissue Proteinsbone diseasesbone tissue engineeringNELL‑1osteogenesis

Identifiers

PMID39450541
PMCPMC11537270

What OpenQuestion holds

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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.