Evidence map›Paper›PMID 31203752›Full record

ArticleAutophagy2020

Loss of autophagy in chondrocytes causes severe growth retardation.

Yoji Horigome, Hiroko Ida-Yonemochi, Satoshi Waguri, Shunichi Shibata, Naoto Endo, Masaaki Komatsu

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
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  12. Autophagic Mediators in Bone Marrow Niche Homeostasis.Advances in experimental medicine and biology · 2022
    Article
  13. Article
  14. Autophagy coordinates chondrocyte development and early joint formation in zebrafish.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Chondrocyte Aging: The Molecular Determinants and Therapeutic Opportunities.Frontiers in cell and developmental biology · 2021
    Review
  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 4 institutions in 1 country.

Yoji HorigomeDepartment of Biochemistry, Niigata University Graduate School of Medical and Dental Sciences, Chuo-ku, Japan.
Hiroko Ida-YonemochiDivision of Anatomy and Cell Biology of the Hard Tissue, Department of Tissue Regeneration and Reconstruction, Niigata University Graduate School of Medical and Dental Sciences, Chuo-ku, Japan.
Satoshi WaguriDepartment of Anatomy and Histology, Fukushima Medical University School of Medicine, Hikarigaoka, Japan.
Shunichi ShibataDepartment of Maxillofacial Anatomy, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.ORCID 0000-0003-3412-7002
Naoto EndoDivision of Orthopedic Surgery Department of Regeneration and Transplant Medicine, Niigata University Graduate School of Medical and Dental Sciences, Chuo-ku, Japan.
Masaaki KomatsuDepartment of Biochemistry, Niigata University Graduate School of Medical and Dental Sciences, Chuo-ku, Japan.ORCID 0000-0001-7672-7722
Niigata University · JPFukushima Medical University · JPJuntendo University · JPTokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chondrogenesis is accompanied by not only cellular renovation, but also metabolic stress. Therefore, macroautophagy/autophagy is postulated to be involved in this process. Previous reports have shown that suppression of autophagy during chondrogenesis causes mild growth retardation. However, the role of autophagy in chondrocyte differentiation still largely remains unclear. Here, we show the important role of autophagy on chondrogenesis. The transition of mesenchymal cells to chondrocytes was severely impaired by ablation of

Indexed as

AutophagyAnimalsCartilageCell LineCell ProliferationChondrocytesEndoplasmic Reticulum StressGlycogenIntegrasesMesodermMice, Inbred C57BLMice, KnockoutOrgan SpecificityPhenotypeSignal TransductionCre recombinaseGlycogenIntegrasesAtg7autophagycartilagechondrogenesisglycogenolysis

Identifiers

PMID31203752
PMCPMC6999621
OpenAlexW2950627492

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.