Evidence map›Paper›PMID 38278996›Full record

ArticleCommunications biology2024

Cortistatin prevents glucocorticoid-associated osteonecrosis of the femoral head via the GHSR1a/Akt pathway.

Yuan Gao, Yunhao You, Pengfei Zhang, Yang Yu, Zhaoning Xu, Hui Wei, Zhicheng Liu, Ruixuan Yu, Gaoxin Jin, Hao Wang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
6.7field-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

12 citing papers in PubMed, 14 citations in OpenAlex.

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  11. The role of the PKCζ/JNK signaling pathway in regulating the development of femoral head necrosis.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025
    Article
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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 3 institutions in 1 country.

Yuan Gao *Department of Orthopedics, Qilu Hospital of Shandong University, Jinan, China.
Yunhao You *Department of Orthopedics, Qilu Hospital of Shandong University, Jinan, China.
Pengfei Zhang *Department of Orthopedics, Qilu Hospital of Shandong University, Jinan, China.ORCID 0000-0003-2621-603X
Yang Yu *Department of Orthopedics, Qilu Hospital of Shandong University, Jinan, China.
Zhaoning XuCheeloo College of Medicine, Shandong University, Jinan, China.ORCID 0000-0001-9237-2626
Hui WeiDepartment of Rehabilitation, Qilu Hospital of Shandong University, Jinan, China.
Zhicheng LiuCheeloo College of Medicine, Shandong University, Jinan, China.
Ruixuan YuDepartment of Orthopedics, Qilu Hospital of Shandong University, Jinan, China.
Gaoxin JinCheeloo College of Medicine, Shandong University, Jinan, China.
Hao WangDepartment of Trauma Orthopedics, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China. wanghaosl@sdfmu.edu.cn.ORCID 0000-0001-6321-2391
Shuai ZhangDepartment of Orthopedics, Qilu Hospital of Shandong University, Jinan, China. zhangshuai1106@126.com.ORCID 0009-0008-1606-5243
Yuhua LiDepartment of Orthopedics, Qilu Hospital of Shandong University, Jinan, China. liyuhua@qiluhospital.com.ORCID 0009-0001-9750-9430
Weiwei LiDepartment of Pathology, Qilu Hospital of Shandong University, Jinan, China. liweiweizhao@163.com.ORCID 0000-0003-3485-164X
Shandong University · CNQilu Hospital of Shandong University · CNShandong Provincial Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81972155National Natural Science Foundation of China (National Science Foundation of China) 82073437
6 · The paper itself

Abstract

Long-term use of glucocorticoids (GCs) is known to be a predominant cause of osteonecrosis of the femoral head (ONFH). Moreover, GCs can mediate apoptosis of various cell types by exaggerating oxidative stress. We have previously found that Cortistatin (CST) antagonizes oxidative stress and improves cell apoptosis in several conditions. In this study, we detected that the CST expression levels were diminished in patients with ONFH compared with femoral neck fracture (FNF). In addition, a GC-induced rat ONFH model was established, which impaired bone quality in the femoral head. Then, administration of CST attenuated these ONFH phenotypes. Furthermore, osteoblast and endothelial cells were cultured and stimulated with dexamethasone (Dex) in the presence or absence of recombinant CST. As a result, Dex induced impaired anabolic metabolism of osteoblasts and suppressed tube formation in endothelial cells, while additional treatment with CST reversed this damage to the cells. Moreover, blocking GHSR1a, a well-accepted receptor of CST, or blocking the AKT signaling pathway largely abolished the protective function of CST in Dex-induced disorder of the cells. Taken together, we indicate that CST has the capability to prevent GC-induced apoptosis and metabolic disorder of osteoblasts in the pathogenesis of ONFH via the GHSR1a/AKT signaling pathway.

Indexed as

GlucocorticoidsNeuropeptidesOsteonecrosisAnimalsEndothelial CellsFemur HeadHumansProto-Oncogene Proteins c-aktRatscortistatinGlucocorticoidsNeuropeptidesProto-Oncogene Proteins c-akt

Identifiers

PMID38278996
PMCPMC10817896
OpenAlexW4391258659

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.