Evidence map›Paper›PMID 42003749›Full record

ReviewFuture science OA2026

The regulatory significance of chondrocyte hypertrophy in maintaining chondrocyte homeostasis, regeneration and repair.

Jingxin Li, Changliang Ma, Wenting Jiang, Xiaoqiang Chen, Jianquan Liu, Xu Tao, Zhe Zhao, Wencui Li, Zhiqin Deng

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Future science OA, 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.

Jingxin LiHand and Foot Surgery Department, Shenzhen Second People's Hospital/the First Hospital Affiliated to Shenzhen University, Medical Innovation Technology Transformation Center of Shenzhen Second People's Hospital, Shenzhen, China.
Changliang MaHand and Foot Surgery Department, Shenzhen Second People's Hospital/the First Hospital Affiliated to Shenzhen University, Medical Innovation Technology Transformation Center of Shenzhen Second People's Hospital, Shenzhen, China.
Wenting JiangOperating Room, Shenzhen Second People's Hospital/the First Hospital Affiliated to Shenzhen University, Shenzhen, China.
Xiaoqiang ChenHand and Foot Surgery Department, Shenzhen Second People's Hospital/the First Hospital Affiliated to Shenzhen University, Medical Innovation Technology Transformation Center of Shenzhen Second People's Hospital, Shenzhen, China.
Jianquan LiuHand and Foot Surgery Department, Shenzhen Second People's Hospital/the First Hospital Affiliated to Shenzhen University, Medical Innovation Technology Transformation Center of Shenzhen Second People's Hospital, Shenzhen, China.
Xu TaoHand and Foot Surgery Department, Shenzhen Second People's Hospital/the First Hospital Affiliated to Shenzhen University, Medical Innovation Technology Transformation Center of Shenzhen Second People's Hospital, Shenzhen, China.
Zhe ZhaoHand and Foot Surgery Department, Shenzhen Second People's Hospital/the First Hospital Affiliated to Shenzhen University, Medical Innovation Technology Transformation Center of Shenzhen Second People's Hospital, Shenzhen, China.ORCID 0000-0001-5511-3764
Wencui LiHand and Foot Surgery Department, Shenzhen Second People's Hospital/the First Hospital Affiliated to Shenzhen University, Medical Innovation Technology Transformation Center of Shenzhen Second People's Hospital, Shenzhen, China.ORCID 0000-0003-2787-5360
Zhiqin DengHand and Foot Surgery Department, Shenzhen Second People's Hospital/the First Hospital Affiliated to Shenzhen University, Medical Innovation Technology Transformation Center of Shenzhen Second People's Hospital, Shenzhen, China.ORCID 0000-0002-0819-8504

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chondrocyte hypertrophy is a pivotal biological process in skeletal development and disease progression, with its precise regulation being essential for maintaining cartilage homeostasis and promoting tissue repair. This review systematically summarizes the molecular mechanisms of chondrocyte hypertrophy and its roles in both physiology and pathology, with a focus on its central involvement in osteoarthritis (OA), growth plate dysplasia, and heterotopic ossification. Key signaling pathways, including RUNX2, BMP, Wnt/β-catenin, and PTHrP, orchestrate hypertrophy through intricate crosstalk. Conversely, inhibitory factors such as SOX9, HIFs, and miRNAs preserve chondrocyte phenotype stability. Pathologically, dysregulated hypertrophy drives cartilage matrix degradation, metabolic reprogramming, and pro-inflammatory microenvironments, thereby exacerbating OA progression. Single-cell omics has unveiled cellular heterogeneity in OA cartilage, and innovative biomaterials combined with stem cell therapies offer promising regenerative approaches. However, limitations persist in understanding pathway interactions, replicating in vivo complexity in vitro, and translating findings to clinical applications. Future research should integrate multidisciplinary technologies to develop precise therapeutic strategies, advancing the treatment of cartilage-related disorders. This review is designed as a

Indexed as

biomaterialsBMP signalingChondrocyte hypertrophyosteoarthritisRUNX2SOX9stem cell therapyWnt/β-catenin pathway

Identifiers

PMID42003749
PMCPMC13097783

What Socratic holds

Textmetadata
LicenceCC BY-NC
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.