Evidence map›Paper›PMID 38609896›Full record

ArticleBMC musculoskeletal disorders2024

FTH1 protects against osteoarthritis by MAPK pathway inhibition of extracellular matrix degradation.

Zhikun Yuan, Lingfeng Yang, Yanhui Li, Xuming Li, Changgui Peng, Jianying Pan, Daozhang Cai

Open access · goldAbstract read
In one paragraph

Article in BMC musculoskeletal disorders, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Evaluating the Anti-Inflammatory and Chondroprotective Effects ofInternational journal of molecular sciences · 2025
    Article
  7. Review
  8. 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

7 authors at 2 institutions in 1 country.

Zhikun Yuan *Department of Orthopedics, Shijie Hospital of Dongguan City, Dongguan, China.
Lingfeng Yang *Department of Orthopedics, Orthopedic Hospital of Guangdong Province, Academy of Orthopedics·Guangdong Province, The Third School of Clinical Medicine, The Third Affiliated Hospital, Southern Medical University, Guangzhou, China.
Yanhui Li *Department of Pathology, Shijie Hospital of Dongguan City, Dongguan, China.
Xuming LiDepartment of Orthopedics, Shijie Hospital of Dongguan City, Dongguan, China.
Changgui PengDepartment of Orthopedics, Shijie Hospital of Dongguan City, Dongguan, China.
Jianying PanDepartment of Orthopedics, Orthopedic Hospital of Guangdong Province, Academy of Orthopedics·Guangdong Province, The Third School of Clinical Medicine, The Third Affiliated Hospital, Southern Medical University, Guangzhou, China. storm0132002@163.com.
Daozhang CaiDepartment of Orthopedics, Orthopedic Hospital of Guangdong Province, Academy of Orthopedics·Guangdong Province, The Third School of Clinical Medicine, The Third Affiliated Hospital, Southern Medical University, Guangzhou, China. cdz@smu.edu.cn.
Dongguan People’s Hospital · CNThird Affiliated Hospital of Southern Medical University · CN

Funding

National Natural Science Foundation of China 8217091163
6 · The paper itself

Abstract

objectiveFerritin heavy chain 1 (FTH1) is an important subunit of ferro-storing proteins and is indispensable for iron metabolism. Though it has been extensively studied in numerous organs and diseases, the relationship between FTH1 and osteoarthritis (OA) is unclear.

designPrimary murine chondrocytes and cartilage explants were treated with FTH1 siRNA for 72 h. Mice were injected with adenovirus expressing FTH1 after destabilized medial meniscus (DMM) surgery. These approaches were used to determine the effect of FTH1 expression on the pathophysiology of OA.

resultsFTH1 expression was down regulated in OA patients and mice after DMM surgery. Knock down of FTH1 induced articular cartilage damage and extracellular matrix degradation in cartilage explants. Further, over expression of FTH1 reduced the susceptibility of chondrocytes to ferroptosis and reversed decrements in SOX9 and aggrecan after DMM surgery. Moreover, FTH1 relieved OA by inhibition of the chondrocyte MAPK pathway.

conclusionThis study found FTH1 to play an essential role in extracellular matrix degradation, ferroptosis, and chondrocytes senescence during OA progression. Further, injection of adenovirus expressing FTH1 may be a potential strategy for OA prevention and therapy.

Indexed as

OsteoarthritisAdenoviridaeAggrecansAnimalsChondrocytesExtracellular MatrixFerritinsHumansMiceOxidoreductasesAggrecansFerritinsFTH1 protein, humanFth1 protein, mouseOxidoreductasesCartilageECMFerroptosisOsteoarthritis

Identifiers

PMID38609896
PMCPMC11010333
OpenAlexW4394753657

What OpenQuestion holds

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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.