Evidence map›Paper›PMID 23479732›Full record

ArticleThe Journal of biological chemistry2013

Deletion of autophagy-related 5 (Atg5) and Pik3c3 genes in the lens causes cataract independent of programmed organelle degradation.

Hideaki Morishita, Satoshi Eguchi, Hirotaka Kimura, Junko Sasaki, Yuriko Sakamaki, Michael L Robinson, Takehiko Sasaki, Noboru Mizushima

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 1 pooled it
8.3field-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

87 citing papers in PubMed, 1 synthesis or guideline pooled it, 151 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Exploiting autophagy and related pathways: pioneering new horizons in cataract therapy.Apoptosis : an international journal on programmed cell death · 2025
    Review
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  19. Article
  20. Autophagy in graves' ophthalmopathy.Frontiers in cell and developmental biology · 2023
    Review

27 more citing papers are in PubMed but not listed here.

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

8 authors at 3 institutions in 2 countries.

Hideaki MorishitaDepartment of Physiology and Cell Biology, Tokyo Medical and Dental University, Tokyo 113-8519, Japan.
Satoshi Eguchi
Hirotaka Kimura
Junko Sasaki
Yuriko Sakamaki
Michael L Robinson
Takehiko Sasaki
Noboru Mizushima
Akita University · JPTokyo Medical and Dental University · JPMiami University · US

Funding

THE ROLE OF FGF RECPETORS IN LENS DEVELOPMENTR01EY012995 · NEI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI ROBINSON, MICHAEL L · 2000 to 2018
$4.9M
NEI NIH HHS R01 EY012995NEI NIH HHS R01EY012995
6 · The paper itself

Abstract

The lens of the eye is composed of fiber cells, which differentiate from epithelial cells and undergo programmed organelle degradation during terminal differentiation. Although autophagy, a major intracellular degradation system, is constitutively active in these cells, its physiological role has remained unclear. We have previously shown that Atg5-dependent macroautophagy is not necessary for lens organelle degradation, at least during the embryonic period. Here, we generated lens-specific Atg5 knock-out mice and showed that Atg5 is not required for lens organelle degradation at any period of life. However, deletion of Atg5 in the lens results in age-related cataract, which is accompanied by accumulation of polyubiquitinated and oxidized proteins, p62, and insoluble crystallins, suggesting a defect in intracellular quality control. We also produced lens-specific Pik3c3 knock-out mice to elucidate the possible involvement of Atg5-independent alternative autophagy, which is proposed to be dependent on Pik3c3 (also known as Vps34), in lens organelle degradation. Deletion of Pik3c3 in the lens does not affect lens organelle degradation, but it leads to congenital cataract and a defect in lens development after birth likely due to an impairment of the endocytic pathway. Taken together, these results suggest that clearance of lens organelles is independent of macroautophagy. These findings also clarify the physiological role of Atg5 and Pik3c3 in quality control and development of the lens, respectively.

Indexed as

AnimalsAutophagyAutophagy-Related Protein 5CataractClass III Phosphatidylinositol 3-KinasesCrystallinsEndocytosisLens Capsule, CrystallineMiceMice, KnockoutMicrotubule-Associated ProteinsOrganellesUbiquitinated ProteinsAtg5 protein, mouseAutophagy-Related Protein 5Class III Phosphatidylinositol 3-KinasesCrystallinsMicrotubule-Associated ProteinsUbiquitinated Proteins

Identifiers

PMID23479732
PMCPMC3630873
OpenAlexW1993784744

What OpenQuestion holds

Textmetadata
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.