Evidence map›Paper›PMID 33379277›Full record

ArticleJournal of clinical medicine2020

Cathepsin B Localizes in the Caveolae and Participates in the Proteolytic Cascade in Trabecular Meshwork Cells. Potential New Drug Target for the Treatment of Glaucoma.

April Nettesheim, Myoung Sup Shim, Angela Dixon, Urmimala Raychaudhuri, Haiyan Gong, Paloma B Liton

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.7field-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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Exploiting autophagy and related pathways: pioneering new horizons in cataract therapy.Apoptosis : an international journal on programmed cell death · 2025
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Evaluation of trabecular meshwork-specific promotersInternational journal of ophthalmology · 2023
    Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. 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

6 authors at 2 institutions in 1 country.

April NettesheimDepartment of Ophthalmology & Pathology, Duke University, Durham, NC 27705, USA.
Myoung Sup ShimDepartment of Ophthalmology & Pathology, Duke University, Durham, NC 27705, USA.ORCID 0000-0001-6535-1416
Angela DixonDepartment of Ophthalmology & Pathology, Duke University, Durham, NC 27705, USA.
Urmimala RaychaudhuriDepartment of Ophthalmology & Pathology, Duke University, Durham, NC 27705, USA.
Haiyan GongDepartment of Ophthalmology, Boston University School of Medicine, Boston, MA 02118, USA.
Paloma B LitonDepartment of Ophthalmology & Pathology, Duke University, Durham, NC 27705, USA.
Duke University · USBoston 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
Cellular Physiology of the Aqueous Outflow PathwayR01EY022634 · NEI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GONG, HAIYAN · 2012 to 2020
$3.7M
Lysosomal Enzymes in Outflow Pathway Physiology and PathophysiologyR01EY027733 · NEI · DUKE UNIVERSITY · PI LITON, PALOMA · 2017 to 2020
$1.8M
NEI NIH HHS EY026885, EY027733, EY005722NEI NIH HHS R01 EY022634NEI NIH HHS R01 EY026885NEI NIH HHS R01 EY027733
6 · The paper itself

Abstract

Extracellular matrix (ECM) deposition in the trabecular meshwork (TM) is one of the hallmarks of glaucoma, a group of human diseases and leading cause of permanent blindness. The molecular mechanisms underlying ECM deposition in the glaucomatous TM are not known, but it is presumed to be a consequence of excessive synthesis of ECM components, decreased proteolytic degradation, or both. Targeting ECM deposition might represent a therapeutic approach to restore outflow facility in glaucoma. Previous work conducted in our laboratory identified the lysosomal enzyme cathepsin B (CTSB) to be expressed on the cellular surface and to be secreted into the culture media in trabecular meshwork (TM) cells. Here, we further investigated the role of CTSB on ECM remodeling and outflow physiology in vitro and in CSTB

Indexed as

cathepsin BECMfibrosisglaucomaPAI-1proteolytic cascadeTGFβtrabecular meshwork

Identifiers

PMID33379277
PMCPMC7795952
OpenAlexW3115325381

What OpenQuestion holds

Textmetadata
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.