Evidence map›Paper›PMID 24583119›Full record

ArticleBiochimica et biophysica acta2014

MTOR-independent induction of autophagy in trabecular meshwork cells subjected to biaxial stretch.

Kristine M Porter, Nallathambi Jeyabalan, Paloma B Liton

Abstract read
In one paragraph

Article in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
–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

47 citing papers in PubMed.

  1. Autophagy in ocular diseases: from mechanisms to therapeutic potential.Frontiers in cell and developmental biology · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. To be or not to be - Decoding the Trabecular Meshwork Cell Identity.bioRxiv : the preprint server for biology · 2024
    Article
  11. Article
  12. Article
  13. A Feedback Loop between TGF-β1 andCurrent issues in molecular biology · 2023
    Article
  14. Article
  15. iPSCs-Based Therapy for Trabecular Meshwork.Handbook of experimental pharmacology · 2023
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
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

3 authors.

Kristine M PorterDuke University, Department of Ophthalmology, Durham, NC, USA.
Nallathambi JeyabalanDuke University, Department of Ophthalmology, Durham, NC, USA.
Paloma B LitonDuke University, Department of Ophthalmology, Durham, NC, USA. Electronic address: paloma.liton@dm.duke.edu.

Funding

VISION RESEARCHP30EY005722 · NEI · DUKE UNIVERSITY · PI Vadim Y Arshavsky · 1985 to 2026
$19.3M
Autophagic Lysosomal Pathway and GlaucomaR01EY020491 · NEI · DUKE UNIVERSITY · PI LITON, PALOMA · 2010 to 2014
$1.5M
NEI NIH HHS P30 EY005722NEI NIH HHS P30EY005722NEI NIH HHS R01 EY020491NEI NIH HHS R01EY020491
6 · The paper itself

Abstract

The trabecular meshwork (TM) is part of a complex tissue that controls the exit of aqueous humor from the anterior chamber of the eye, and therefore helps maintaining intraocular pressure (IOP). Because of variations in IOP with changing pressure gradients and fluid movement, the TM and its contained cells undergo morphological deformations, resulting in distention and stretching. It is therefore essential for TM cells to continuously detect and respond to these mechanical forces and adapt their physiology to maintain proper cellular function and protect against mechanical injury. Here we demonstrate the activation of autophagy, a pro-survival pathway responsible for the degradation of long-lived proteins and organelles, in TM cells when subjected to biaxial static stretch (20% elongation), as well as in high-pressure perfused eyes (30mmHg). Morphological and biochemical markers for autophagy found in the stretched cells include elevated LC3-II levels, increased autophagic flux, and the presence of autophagic figures in electron micrographs. Furthermore, our results indicate that the stretch-induced autophagy in TM cells occurs in an MTOR- and BAG3-independent manner. We hypothesize that activation of autophagy is part of the physiological response that allows TM cells to cope and adapt to mechanical forces.

Indexed as

AutophagyStress, MechanicalAdaptor Proteins, Signal TransducingAnimalsApoptosis Regulatory ProteinsBlotting, WesternCells, CulturedHumansIntraocular PressureLysosomesMicrotubule-Associated ProteinsOrgan Culture TechniquesRNA, Small InterferingSwineTOR Serine-Threonine KinasesTrabecular MeshworkAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsBAG3 protein, humanMAP1LC3A protein, humanMicrotubule-Associated ProteinsMTOR protein, humanRNA, Small InterferingTOR Serine-Threonine KinasesAutophagyChaperon-assisted autophagyGlaucomaMechanical stressMTOR pathwayTrabecular meshwork

Identifiers

PMID24583119
PMCPMC3988584

What OpenQuestion holds

Textmetadata
LicenceTDM
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.