Evidence map›Paper›PMID 37511956›Full record

ArticleLife (Basel, Switzerland)2023

Sigma-1 Receptor Activation Is Protective against TGFβ2-Induced Extracellular Matrix Changes in Human Trabecular Meshwork Cells.

Minh Ngoc Tran, Timea Medveczki, Balazs Besztercei, Gyorgy Torok, Attila J Szabo, Xavier Gasull, Illes Kovacs, Andrea Fekete, Judit Hodrea

Open access · goldAbstract read
In one paragraph

Article in Life (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Sigma-1 Receptor as a Novel Therapeutic Target in Diabetic Kidney Disease.International journal of molecular sciences · 2024
    Article
  5. 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

9 authors at 2 institutions in 4 countries.

Minh Ngoc TranMTA-SE Lendület "Momentum" Diabetes Research Group, Semmelweis University, 1083 Budapest, Hungary.ORCID 0000-0002-6925-0871
Timea MedveczkiMTA-SE Lendület "Momentum" Diabetes Research Group, Semmelweis University, 1083 Budapest, Hungary.
Balazs BeszterceiInstitute of Clinical Experimental Research, Semmelweis University, 1094 Budapest, Hungary.
Gyorgy TorokDepartment of Biophysics and Radiation Biology, Semmelweis University, 1094 Budapest, Hungary.ORCID 0000-0001-7616-5782
Attila J SzaboSemmelweis University Pediatric Center, MTA Center of Excellence, 1083 Budapest, Hungary.
Xavier GasullDepartment of Biomedicine, Institute of Neurosciences, University of Barcelona, 08035 Barcelona, Spain.ORCID 0000-0002-6154-8323
Illes KovacsDepartment of Ophthalmology, Semmelweis University, 1085 Budapest, Hungary.
Andrea FeketeMTA-SE Lendület "Momentum" Diabetes Research Group, Semmelweis University, 1083 Budapest, Hungary.
Judit HodreaMTA-SE Lendület "Momentum" Diabetes Research Group, Semmelweis University, 1083 Budapest, Hungary.
Semmelweis University · HUUniversitat de Barcelona · ES

Funding

Hungarian Academy of Sciences LP2021-3/2021Hungarian Scientific Research Fund OTKA- K135398Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund TKP2021-EGA-24
6 · The paper itself

Abstract

The trabecular meshwork (TM) route is the principal outflow egress of the aqueous humor. Actin cytoskeletal remodeling in the TM and extracellular matrix (ECM) deposition increase TM stiffness, outflow resistance, and elevate intraocular pressure (IOP). These alterations are strongly linked to transforming growth factor-β2 (TGFβ2), a known profibrotic cytokine that is markedly elevated in the aqueous humor of glaucomatous eyes. Sigma-1 receptor (S1R) has been shown to have neuroprotective effects in the retina, but data are lacking about its role in the TM. In this study, we identified the presence of S1R in mouse TM tissue and investigated the effect of an S1R agonist fluvoxamine (FLU) on TGFβ2-induced human TM cells regarding cell proliferation; ECM-related functions, including F-actin reorganization; and the accumulation of ECM elements. TGFβ2 increased the proliferation, cytoskeletal remodeling, and protein levels of fibronectin, collagen type IV, and connective tissue growth factor, and decreased the level of matrix metalloproteinase-2. Most importantly, FLU reversed all these effects of TGFβ2, suggesting that S1R agonists could be potential candidates for preserving TM function and thus maintaining normal IOP.

Indexed as

cytoskeletal remodelingextracellular matrixfluvoxamineglaucomaintraocular pressureoutflow pathway resistanceproliferationSigma-1 receptorTGFβ2trabecular meshwork

Identifiers

PMID37511956
PMCPMC10381521
OpenAlexW4385377624

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.