Evidence map›Paper›PMID 33190410›Full record

ArticleFEBS open bio2021

Glucocorticoids induce femoral head necrosis in rats through the ROS/JNK/c-Jun pathway.

Puji Peng, Zhigang Nie, Fei Sun, Hao Peng

Abstract read
In one paragraph

Article in FEBS open bio, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
–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

40 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. [Mechanisms of RNA-binding protein phase separation in steroid-associated necrosis of the femoral head].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
    Review
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  10. 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
  11. Drug design, development and therapy · 2025
    Article
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  13. Article
  14. Review
  15. Article
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  17. Article
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  20. The role and mechanisms of cordycepin in inhibiting cancer cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024
    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

4 authors.

Puji PengDepartment of Orthopedics, Renmin Hospital of Wuhan University, China.ORCID 0000-0003-2345-9810
Zhigang NieDepartment of Orthopedics, Renmin Hospital of Wuhan University, China.ORCID 0000-0002-5132-2224
Fei SunDepartment of Orthopedics, Renmin Hospital of Wuhan University, China.ORCID 0000-0001-6937-4965
Hao PengDepartment of Orthopedics, Renmin Hospital of Wuhan University, China.ORCID 0000-0001-8765-2826

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteonecrosis of the femoral head (ONFH) is a common clinical disease with a high disability rate. Apoptosis of osteoblasts caused by high-dose short-term or low-dose long-term glucocorticoid (GC) administration is the biological basis of steroid-induced avascular necrosis of the femoral head (SANFH). The pathogenesis of SANFH has not yet been fully elucidated, and there is currently a lack of effective clinical treatments. Here, we investigated the role of the reactive oxygen species (ROS)/JNK/c-Jun signaling pathway in SANFH. Dexamethasone (Dex) was used to induce apoptosis in osteoblasts, and this resulted in a significant increase in levels of p-JNK, p-c-Jun, Bax, caspase-3, caspase-9, cytochrome C, Beclin-1, and LC3, and a decrease in levels of P62 and Bcl-2. In addition, intracellular ROS levels were increased and mitochondrial membrane potential was decreased. Administration of 3-MA, an autophagy inhibitor, attenuated Dex-mediated changes in autophagy and apoptosis. A rat model of ONFH exhibited severe bone trabecular hollow bone pits along with a significant increase in femoral head cell apoptosis compared with the control group. Additionally, micro-CT analysis showed that both bone tissue content and femoral head integrity were significantly reduced in the ONFH group. Furthermore, 3-MA treatment decreased the effect of Dex on GC-induced ONFH and osteoblast apoptosis in rats and could counteract microstructure destruction due to femoral head necrosis. In summary, our data suggest that GC can induce osteoblast apoptosis and autophagy through the ROS/JNK/c-Jun signaling pathway, which contributes to ONFH.

Indexed as

AnimalsApoptosisAutophagyDexamethasoneDisease Models, AnimalFemur HeadFemur Head NecrosisGlucocorticoidsHumansMaleMAP Kinase Signaling SystemOsteoblastsProto-Oncogene Proteins c-junRatsReactive Oxygen SpeciesDexamethasoneGlucocorticoidsProto-Oncogene Proteins c-junReactive Oxygen Speciesapoptosisautophagyhormonal osteonecrosis of the femoral headJNK/c-Jun signaling pathwayROS

Identifiers

PMID33190410
PMCPMC7780117

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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.