Evidence map›Paper›PMID 25483712›Full record

ArticleBiochimica et biophysica acta2015

Autophagic dysregulation in glaucomatous trabecular meshwork cells.

Kristine Porter, Joshua Hirt, W Daniel Stamer, Paloma B Liton

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

54 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Protein misfolding and mitochondrial dysfunction in glaucoma.Frontiers in cell and developmental biology · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Modeling complex age-related eye disease.Progress in retinal and eye research · 2024
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Calcium-Signalling in Human Glaucoma Lamina Cribrosa Myofibroblasts.International journal of molecular sciences · 2023
    Review
  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

4 authors at 1 institution in 1 country.

Kristine PorterDuke University, Department of Ophthalmology, Durham, NC, USA.
Joshua HirtDuke University, Department of Ophthalmology, Durham, NC, USA.
W Daniel StamerDuke University, Department of Ophthalmology, Durham, NC, USA.
Paloma B LitonDuke University, Department of Ophthalmology, Durham, NC, USA. Electronic address: paloma.liton@dm.duke.edu.
Duke University · US

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 R01 EY020491
6 · The paper itself

Abstract

Primary open angle glaucoma (POAG) is a degenerative disease commonly associated with aging and elevated intraocular pressure (IOP). Higher resistance to aqueous humor (AH) outflow through the trabecular meshwork (TM) generates the elevated IOP in POAG; unfortunately the underlying molecular mechanisms responsible for elevated resistance are unknown. It is widely accepted, however, that differences between normal and POAG TM tissues are presumably a consequence of cellular dysfunction. Here, we investigated the autophagic function and response to chronic oxidative stress in TM cells isolated from glaucomatous and age-matched donor eyes. Glaucomatous TM cells showed elevated senescence-associated-beta-galactosidase (SA-β-Gal) and cellular lipofuscin, together with decreased steady-state levels of LC3B-II, decreased levels of pRPS6K-T389 and reduced proteolysis of long-live proteins. Moreover, the glaucomatous cultures failed to activate autophagy when exposed to hyperoxic conditions. These results strongly suggest mTOR-dependent dysregulation of the autophagic pathway in cells isolated from the glaucomatous TM. Such dysregulated autophagic capacity can have a detrimental impact in outflow pathway tissue, i.e. mechanotransduction, and thus represent an important factor contributing to the progression of the disease.

Indexed as

AutophagyOxidative StressProteolysisCells, CulturedEye ProteinsGlaucoma, Open-AngleHumansIntraocular PressureTrabecular MeshworkEye ProteinsAutophagyGlaucomaLysosomal proteolysismTOROxidative stressTrabecular meshwork

Identifiers

PMID25483712
PMCPMC4312735
OpenAlexW2038143181

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.