Evidence map›Paper›PMID 31695131›Full record

ArticleScientific reports2019

Transcriptome analysis reveals autophagy as regulator of TGFβ/Smad-induced fibrogenesis in trabecular meshwork cells.

April Nettesheim, Myoung Sup Shim, Josh Hirt, Paloma B Liton

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. 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
2.4field-weighted citation impact, top 11% 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, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Lysosomes in retinal health and disease.Trends in neurosciences · 2023
    Review
  9. Article
  10. A Feedback Loop between TGF-β1 andCurrent issues in molecular biology · 2023
    Article
  11. Calcium-Signalling in Human Glaucoma Lamina Cribrosa Myofibroblasts.International journal of molecular sciences · 2023
    Review
  12. Article
  13. Article
  14. Regulation of TGF-Cancers · 2022
    Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Immune responses to injury and their links to eye disease.Translational research : the journal of laboratory and clinical medicine · 2021
    Review
  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.

April NettesheimDuke University, Department of Ophthalmology, Durham, NC, USA.
Myoung Sup ShimDuke University, Department of Ophthalmology, Durham, NC, USA.
Josh HirtDuke University, Department of Ophthalmology, Durham, NC, USA.
Paloma B LitonDuke University, Department of Ophthalmology, Durham, NC, USA. paloma.liton@dm.duke.edu.
Duke University · US

Funding

VISION RESEARCHP30EY005722 · NEI · DUKE UNIVERSITY · PI Vadim Y Arshavsky · 1985 to 2026
$19.3M
Autophagy and Mechanotransduction in the Trabecular MeshworkR01EY026885 · NEI · DUKE UNIVERSITY · PI Paloma Liton · 2016 to 2026
$4.7M
Lysosomal Enzymes in Outflow Pathway Physiology and PathophysiologyR01EY027733 · NEI · DUKE UNIVERSITY · PI LITON, PALOMA · 2017 to 2020
$1.8M
NEI NIH HHS P30 EY005722NEI NIH HHS R01 EY026885NEI NIH HHS R01 EY027733
6 · The paper itself

Abstract

The trabecular meshwork (TM) is a specialized ocular tissue, which is responsible, together with the Schlemm's canal (SC), for maintaining appropriate levels of intraocular pressure. Dysfunction of these tissues leads to ocular hypertension and increases the risk for developing glaucoma. Previous work by our laboratory revealed dysregulated autophagy in aging and in glaucomatous TM cells. In order to gain more insight in the role of autophagy in the TM pathophysiology, we have conducted transcriptome and functional network analyses of TM primary cells with silenced expression of the autophagy genes Atg5 and Atg7. Atg5/7-deficient TM cells showed changes in transcript levels of several fibrotic genes, including TGFβ2, BAMBI, and SMA. Furthermore, genetic and pharmacological inhibition of autophagy was associated with a parallel reduction in TGFβ-induced fibrosis, caused by a BAMBI-mediated reduced activation of Smad2/3 signaling in autophagy-deficient cells. At the same time, TGFβ treatment led to Smad2/3-dependent dysregulation of autophagy in TM cells, characterized by increased LC3-II levels and autophagic vacuoles content. Together, our results indicate a cross-talk between autophagy and TGFβ signaling in TM cells.

Indexed as

AutophagyAutophagy-Related Protein 5Autophagy-Related Protein 7Cells, CulturedFibrosisHumansMembrane ProteinsSmad2 ProteinSmad3 ProteinTrabecular MeshworkTransforming Growth Factor beta2Autophagy-Related Protein 5Autophagy-Related Protein 7BAMBI protein, humanMembrane ProteinsSmad2 ProteinSmad3 ProteinTransforming Growth Factor beta2

Identifiers

PMID31695131
PMCPMC6834604
OpenAlexW2987564467

What OpenQuestion holds

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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.