Evidence map›Paper›PMID 37309689›Full record

ArticleCell proliferation2023

Endothelial Stat3 activation promotes osteoarthritis development.

Jiadong Li, Wencai Zhang, Xinru Liu, Guangfeng Li, Yuyuan Gu, Kun Zhang, Fuming Shen, Xiang Wu, Yingying Jiang, Qin Zhang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
7.0field-weighted citation impact, top 2% of its field
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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

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  16. The regulatory roles of STAT3 protein in the pathogenesis of viral infections.Frontiers in cellular and infection microbiology · 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

13 authors at 4 institutions in 1 country.

Jiadong LiInstitute of Translational Medicine, Shanghai University, Shanghai, China.
Wencai ZhangDepartment of Orthopedics, First Affiliated Hospital, Jinan University, Guangzhou, China.
Xinru LiuInstitute of Translational Medicine, Shanghai University, Shanghai, China.
Guangfeng LiDepartment of Orthopedics, Shanghai Zhongye Hospital, Shanghai, China.
Yuyuan GuInstitute of Translational Medicine, Shanghai University, Shanghai, China.
Kun ZhangDepartment of Orthopedics, Honghui Hospital, Xi'an Jiao Tong University, Xi'an, China.
Fuming ShenInstitute of Translational Medicine, Shanghai University, Shanghai, China.
Xiang WuInstitute of Translational Medicine, Shanghai University, Shanghai, China.
Yingying JiangInstitute of Translational Medicine, Shanghai University, Shanghai, China.ORCID https://orcid.org/0000-0002-0788-8546
Qin ZhangInstitute of Translational Medicine, Shanghai University, Shanghai, China.
Fengjin ZhouDepartment of Orthopedics, Honghui Hospital, Xi'an Jiao Tong University, Xi'an, China.
Ke XuInstitute of Translational Medicine, Shanghai University, Shanghai, China.
Jiacan SuInstitute of Translational Medicine, Shanghai University, Shanghai, China.ORCID https://orcid.org/0000-0001-7080-263X
Shanghai University · CNXi'an Honghui Hospital · CNFirst Affiliated Hospital of Jinan University · CNZhongshan Hospital · CN

Funding

Key Project of the National Natural Science Foundation of China 82230071National Natural Science Foundation of China 32101084National Natural Science Foundation of China 82172098
6 · The paper itself

Abstract

The mechanism of the balance between subchondral angiogenesis and articular damage within osteoarthritis (OA) progression remains a mystery. However, the lack of specific drugs leads to limited clinical treatment options for OA, frequently failing to prevent eventual joint destruction in patients. Increasing evidence suggests that subchondral bone angiogenesis precedes cartilage injury, while proliferating endothelial cells (ECs) induce abnormal bone formation. Signal transducer and activator of transcription 3 (Stat3) is triggered by multiple cytokines in the OA microenvironment. Here, we observed elevated Stat3 activation in subchondral bone H-type vessels. Endothelial Stat3 activation will lead to stronger cell proliferation, migration and angiogenesis by simulating ECs in OA. In contrast, either Stat3 activation inhibition or knockdown of Stat3 expression could relieve such alterations. More interestingly, blocking Stat3 in ECs alleviated angiogenesis-mediated osteogenic differentiation and chondrocyte lesions. Stat3 inhibitor reversed surgically induced subchondral bone H-type vessel hyperplasia in vivo, significantly downregulating vessel volume and vessel number. Due to the reduced angiogenesis, subchondral bone deterioration and cartilage loss were alleviated. Overall, our data suggest that endothelial Stat3 activation is an essential trigger for OA development. Therefore, targeted Stat3 blockade is a novel promising therapeutic regimen for OA.

Indexed as

Cartilage, ArticularOsteoarthritisSTAT3 Transcription FactorEndothelial CellsHumansOsteogenesisSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID37309689
PMCPMC10693181
OpenAlexW4380422086

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.