Evidence map›Paper›PMID 42337938›Full record

ArticleAging cell2026

Sustained Hypoxia-Inducible Factor 1-Alpha Accumulation Disrupts the Articular Niche to Promote Osteoarthritis Pathogenesis.

Weiyuan Gong, Chu Tao, Xingyun Wang, Rongdong Liao, Jianglong Li, Xiongtian Guo, Minghao Qu, Jianmei Huang, Mingjue Chen, Fuxin Wei and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging cell, 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. 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

16 authors.

Weiyuan GongDepartment of Biomedical Engineering, The Hong Kong Polytechnic University, Hong Kong, China.ORCID https://orcid.org/0009-0003-2667-6973
Chu TaoShenzhen Key Laboratory of Bone Tissue Repair and Translational Research, Department of Orthopaedic Surgery, The Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, China.ORCID https://orcid.org/0009-0003-6069-880X
Xingyun WangDepartment of Pharmacology, School of Medicine, Southern University of Science and Technology, Shenzhen, China.
Rongdong LiaoSichuan Provincial People's Hospital, Sichuan Academy of Medical Sciences, Chengdu, China.ORCID https://orcid.org/0000-0001-9846-6519
Jianglong LiDepartment of Biochemistry, School of Medicine, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China.
Xiongtian GuoShenzhen Key Laboratory of Bone Tissue Repair and Translational Research, Department of Orthopaedic Surgery, The Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, China.
Minghao QuDepartment of Biochemistry, School of Medicine, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China.
Jianmei HuangDepartment of Biochemistry, School of Medicine, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China.
Mingjue ChenDepartment of Biochemistry, School of Medicine, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China.
Fuxin WeiShenzhen Key Laboratory of Bone Tissue Repair and Translational Research, Department of Orthopaedic Surgery, The Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, China.
Peng WangDepartment of Pharmacology, School of Medicine, Southern University of Science and Technology, Shenzhen, China.
Lijun LinDepartment of Joint and Orthopedics, Zhujiang Hospital, Southern Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0002-4077-1198
Di ChenFaculty of Pharmaceutical Sciences, Shenzhen Institute of Advanced Technology, Shenzhen, China.
Qing YaoDepartment of Biochemistry, School of Medicine, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China.
Chunyi WenDepartment of Biomedical Engineering, The Hong Kong Polytechnic University, Hong Kong, China.
Guozhi XiaoDepartment of Biochemistry, School of Medicine, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Southern University of Science and Technology, Shenzhen, China.

Funding

Guangdong Provincial Science and Technology Innovation Council Grant 2017B030301018National Natural Science Foundation of China Grants 82230081National Natural Science Foundation of China Grants 82250710175National Natural Science Foundation of China Grants 82261160395National Natural Science Foundation of China Grants 82430078Noncommunicable Chronic Diseases-National Science and Technology Major Project 2025ZD0550400Science and Technology Innovation Commission of Shenzhen Municipal Government Grants ZDSYS20140509142721429Shenzhen Medical Research Funds B2402033Shenzhen Medical Research Funds B2504003Shenzhen Medical Research Funds E250200210
6 · The paper itself

Abstract

The precise role of hypoxia-inducible factor-1α (HIF-1α) in osteoarthritis (OA) pathogenesis remains controversial, often debated between a protective compensatory factor and a disease mediator. Here, we demonstrate that sustained, uncoupled HIF-1α accumulation functions as a potent, compartment-specific pathogenic driver of joint destruction. Using genetically engineered mouse models, we reveal that chondrocyte-specific HIF-1α overexpression (Acan

Indexed as

Cartilage, ArticularHypoxia-Inducible Factor 1, alpha SubunitOsteoarthritisAnimalsChondrocytesDisease Models, AnimalHumansMaleMiceHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitcartilageHIF‐1αLNP‐mRNAOA

Identifiers

PMID42337938
PMCPMC13290656

What OpenQuestion 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 OpenQuestion graph.