Evidence map›Paper›PMID 35560791›Full record

ReviewJournal of cellular and molecular medicine2022

Targeted regulation of FoxO1 in chondrocytes prevents age-related osteoarthritis via autophagy mechanism.

Jiaji Yue, Aikebaier Aobulikasimu, Weichao Sun, Shuyu Liu, Wei Xie, Wei Sun

Open access · goldAbstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Forkhead box O proteins in chondrocyte aging and diseases.Journal of orthopaedic translation · 2025
    Review
  8. Article
  9. Review
  10. The link of FOXO1 and FOXO4 transcription factors to development of the lens.Developmental dynamics : an official publication of the American Association of Anatomists · 2025
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

Jiaji YueDepartment of Bone and Joint Surgery, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, China.ORCID 0000-0001-8113-4577
Aikebaier AobulikasimuDepartment of Bone and Joint Surgery, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, China.
Weichao SunDepartment of Bone and Joint Surgery, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, China.
Shuyu LiuDepartment of Bone and Joint Surgery, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, China.
Wei XieDepartment of Bone and Joint Surgery, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, China.
Wei SunDepartment of Bone and Joint Surgery, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, China.
Shenzhen Second People's Hospital · CN

Funding

Guangdong Medical Research Foundation A2021321Shenzhen High-level Hospital Construction Fund-Orthopedic GK202203007
6 · The paper itself

Abstract

Autophagy is designated as a biological recycling process to maintain cellular homeostasis by the sequestration of damaged proteins and organelles in plasma and cargo delivery to lysosomes for degradation and reclamation. This organelle recycling process promotes chondrocyte homeostasis and has been previously implicated in osteoarthritis (OA). Autophagy is widely involved in regulating chondrocyte degeneration markers such as MMPs, ADAMSTs and Col10 in chondrocytes. The critical autophagy-related (ATG) proteins have now been considered the protective factor against late-onset OA. The current research field proposes that the autophagic pathway is closely related to chondrocyte activity. However, the mechanism is complex yet needs precise elaboration. This review concluded that FoxO1, a forkhead O family protein, which is a decisive mediator of autophagy, facilitates the pathological process of osteoarthritis. Diverse mechanisms regulate the activity of FoxO1 and promote the initiation of autophagy, including the prominent AMPK and Sirt-2 cellular pathways. FoxO1 transactive is regulated by phosphorylation and acetylation processes, which modulates the downstream ATGs expression. Furthermore, FoxO1 induces autophagy by directly interacting with ATGs proteins, which control the formation of autophagosomes and lysosomes fusion. This review will discuss cutting-edge evidence that the FoxO-autophagy pathway plays an essential regulator in the pathogenesis of osteoarthritis.

Indexed as

Cartilage, ArticularOsteoarthritisAutophagyChondrocytesForkhead Box Protein O1Forkhead Transcription FactorsHumansForkhead Box Protein O1Forkhead Transcription FactorsFOXO1 protein, humanautophagychondrocytesFoxO1osteoarthritis

Identifiers

PMID35560791
PMCPMC9170816
OpenAlexW4280594209

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.