Evidence map›Paper›PMID 40391077›Full record

ArticleOpen medicine (Warsaw, Poland)2025

Celastrol suppresses neovascularization in rat aortic vascular endothelial cells stimulated by inflammatory tenocytes via modulating the NLRP3 pathway.

Yong Yang, Huajun Wang, Huige Hou, Jiwen Chen, Xiaolei Chen, Hongjian Zheng, Kai Zheng, Baofei Ye, Chunhui Wu, Xiaofei Zheng and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Open medicine (Warsaw, Poland), 2025. 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

12 authors.

Yong YangDepartment of Orthopedics, The Affiliated Shunde Hospital of Jinan University, Foshan, Guangdong Province, China.
Huajun WangDepartment of Sports Medicine, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Speed Capability, The Guangzhou Key Laboratory of Precision Orthopedics and Regenerative Medicine, Jinan University, 510630, Guangzhou, China.
Huige HouDepartment of Sports Medicine, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Speed Capability, The Guangzhou Key Laboratory of Precision Orthopedics and Regenerative Medicine, Jinan University, 510630, Guangzhou, China.
Jiwen ChenDepartment of Orthopedics, The Affiliated Shunde Hospital of Jinan University, Foshan, Guangdong Province, China.
Xiaolei ChenDepartment of Orthopedics, The Affiliated Shunde Hospital of Jinan University, Foshan, Guangdong Province, China.
Hongjian ZhengDepartment of Orthopedics, The Affiliated Shunde Hospital of Jinan University, Foshan, Guangdong Province, China.
Kai ZhengDepartment of Orthopaedic, Hainan Hospital, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, China.
Baofei YeDepartment of Orthopaedic, Hainan Hospital, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, China.
Chunhui WuDepartment of Orthopedics, The Affiliated Shunde Hospital of Jinan University, Foshan, Guangdong Province, China.
Xiaofei ZhengDepartment of Sports Medicine, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Speed Capability, The Guangzhou Key Laboratory of Precision Orthopedics and Regenerative Medicine, Jinan University, 510630, Guangzhou, China.
Shiguo YuanDepartment of Orthopaedic, Hainan Hospital, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, China.
Boyuan ZhengDepartment of Sports Medicine, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Speed Capability, The Guangzhou Key Laboratory of Precision Orthopedics and Regenerative Medicine, Jinan University, 510630, Guangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Appropriate formation of blood vessels is critical for tendon-bone healing during tendon injury, as excessive angiogenesis would exacerbate scar formation and lead to chronic pain and dysfunction. The mechanism to regulate inflammatory angiogenesis during tendon-bone healing remains to be elucidated. Here, we utilized lipopolysaccharide (LPS) to induce tenocyte inflammation and applied the conditioned medium from inflammatory tenocytes to treat rat aortic vascular endothelial cells (RAOECs). The results that indicated LPS treatment significantly induced the mRNA and protein upregulation of NLRP3, tumor necrosis factor α, IL-1β, and vascular endothelial growth factor A (VEGFA), as well as the secretion of VEGFA. Furthermore, the conditioned medium stimulated RAOEC angiogenesis. Celastrol, a quinone-methylated triterpenoid from

Indexed as

angiogenesiscelastrolinflammationneovascularizationNLRP3rotator cuff teartenocytes

Identifiers

PMID40391077
PMCPMC12086628

What OpenQuestion holds

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Registered trials

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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.