Evidence map›Paper›PMID 38902808›Full record

ReviewMilitary Medical Research2024

Role of signaling pathways in age-related orthopedic diseases: focus on the fibroblast growth factor family.

Heng-Zhen Li, Jing-Lve Zhang, Dong-Liang Yuan, Wen-Qing Xie, Christoph H Ladel, Ali Mobasheri, Yu-Sheng Li

Abstract readReview
In one paragraph

Review in Military Medical Research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing 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

35 citing papers in PubMed.

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  18. Klf5a in Endoderm Promotes Pharyngeal Cartilage Morphogenesis.International journal of molecular sciences · 2025
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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

7 authors.

Heng-Zhen Li *Department of Orthopedics, Xiangya Hospital, Central South University, Changsha, 410008, China.
Jing-Lve Zhang *Department of Plastic and Cosmetic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, China.
Dong-Liang YuanDepartment of Orthopedics, Xiangya Hospital, Central South University, Changsha, 410008, China.
Wen-Qing XieDepartment of Orthopedics, Xiangya Hospital, Central South University, Changsha, 410008, China.
Christoph H LadelCHL4special consulting, 64291, Darmstadt, Germany. christoph.ladel@gmail.com.
Ali MobasheriFaculty of Medicine, Research Unit of Health Sciences and Technology, University of Oulu, 90014, Oulu, Finland. ali.mobasheri@oulu.fi.
Yu-Sheng LiDepartment of Orthopedics, Xiangya Hospital, Central South University, Changsha, 410008, China. liyusheng@csu.edu.cn.

Funding

Innovation-Driven Project of Central South University 2020CX045National Key R&D Program of China 2019YFA0111900National Natural Science Foundation of China 82072506National Natural Science Foundation of China 92268115Provincial Clinical Medical Technology Innovation Project of Hunan 2020SK53709Science and Technology Innovation Program of Hunan Province 2021RC3025the Administration of Traditional Chinese Medicine of Hunan Province 2021075the Hunan Provincial Innovation Foundation for Postgraduate No.CX20220350the Independent Exploration and Innovation Project for Postgraduate Students of Central South University No.2022ZZTS0268the program of Health Commission of Hunan Province 202204074879
6 · The paper itself

Abstract

Fibroblast growth factor (FGF) signaling encompasses a multitude of functions, including regulation of cell proliferation, differentiation, morphogenesis, and patterning. FGFs and their receptors (FGFR) are crucial for adult tissue repair processes. Aberrant FGF signal transduction is associated with various pathological conditions such as cartilage damage, bone loss, muscle reduction, and other core pathological changes observed in orthopedic degenerative diseases like osteoarthritis (OA), intervertebral disc degeneration (IVDD), osteoporosis (OP), and sarcopenia. In OA and IVDD pathologies specifically, FGF1, FGF2, FGF8, FGF9, FGF18, FGF21, and FGF23 regulate the synthesis, catabolism, and ossification of cartilage tissue. Additionally, the dysregulation of FGFR expression (FGFR1 and FGFR3) promotes the pathological process of cartilage degradation. In OP and sarcopenia, endocrine-derived FGFs (FGF19, FGF21, and FGF23) modulate bone mineral synthesis and decomposition as well as muscle tissues. FGF2 and other FGFs also exert regulatory roles. A growing body of research has focused on understanding the implications of FGF signaling in orthopedic degeneration. Moreover, an increasing number of potential targets within the FGF signaling have been identified, such as FGF9, FGF18, and FGF23. However, it should be noted that most of these discoveries are still in the experimental stage, and further studies are needed before clinical application can be considered. Presently, this review aims to document the association between the FGF signaling pathway and the development and progression of orthopedic diseases. Besides, current therapeutic strategies targeting the FGF signaling pathway to prevent and treat orthopedic degeneration will be evaluated.

Indexed as

Fibroblast Growth FactorsOsteoarthritisSignal TransductionAgingAnimalsFibroblast Growth Factor-23HumansIntervertebral Disc DegenerationOsteoporosisSarcopeniaFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsFibroblast growth factor (FGF)Fibroblast growth factor receptor (FGFR)Intervertebral disc degeneration (IVDD)Orthopedic degenerationOsteoarthritis (OA)Osteoporosis (OP)Sarcopenia

Identifiers

PMID38902808
PMCPMC11191355

What Socratic holds

Textmetadata
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.