Evidence map›Paper›PMID 37511406›Full record

ArticleInternational journal of molecular sciences2023

Sigma-1 Receptor Agonist Fluvoxamine Ameliorates Fibrotic Response of Trabecular Meshwork Cells.

Judit Hodrea, Minh Ngoc Tran, Balazs Besztercei, Timea Medveczki, Attila J Szabo, Laszlo Őrfi, Illes Kovacs, Andrea Fekete

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

7 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Sigma-1 Receptor as a Novel Therapeutic Target in Diabetic Kidney Disease.International journal of molecular sciences · 2024
    Article
  7. 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

8 authors at 1 institution in 2 countries.

Judit HodreaMTA-SE Lendület "Momentum" Diabetes Research Group, Semmelweis University, 1083 Budapest, Hungary.
Minh Ngoc TranMTA-SE Lendület "Momentum" Diabetes Research Group, Semmelweis University, 1083 Budapest, Hungary.ORCID 0000-0002-6925-0871
Balazs BeszterceiInstitute of Clinical Experimental Research, Semmelweis University, 1094 Budapest, Hungary.
Timea MedveczkiMTA-SE Lendület "Momentum" Diabetes Research Group, Semmelweis University, 1083 Budapest, Hungary.
Attila J SzaboPediatric Center, MTA Center of Excellence, Faculty of Medicine, Semmelweis University, 1083 Budapest, Hungary.ORCID 0000-0001-7321-9861
Laszlo ŐrfiDepartment of Pharmaceutical Chemistry, Semmelweis University, 1092 Budapest, Hungary.ORCID 0000-0001-6149-2385
Illes KovacsDepartment of Ophthalmology, Semmelweis University, 1085 Budapest, Hungary.ORCID 0000-0001-5763-0482
Andrea FeketeMTA-SE Lendület "Momentum" Diabetes Research Group, Semmelweis University, 1083 Budapest, Hungary.
Semmelweis University · HU

Funding

Hungarian Academy of Sciences LP2021-3/2021Hungarian Scientific Research Fund OTKA- K135398the Ministry of Innovation and Technology of Hungary from the National Research, Develop-ment and Innovation Fund TKP2021-EGA-24
6 · The paper itself

Abstract

Primary open-angle glaucoma remains a global issue, lacking a definitive treatment. Increased intraocular pressure (IOP) is considered the primary risk factor of the disease and it can be caused by fibrotic-like changes in the trabecular meshwork (TM) such as increased tissue stiffness and outflow resistance. Previously, we demonstrated that the sigma-1 receptor (S1R) agonist fluvoxamine (FLU) has anti-fibrotic properties in the kidney and lung. In this study, the localization of the S1R in TM cells was determined, and the anti-fibrotic efficacy of FLU was examined in both mouse and human TM cells. Treatment with FLU reduced the F-actin rearrangement, inhibited cell proliferation and migration induced by the platelet-derived growth factor and decreased the levels of fibrotic proteins. The protective role of the S1R in fibrosis was confirmed by a more pronounced increase in alpha smooth muscle actin and F-actin bundle and clump formation in primary mouse S1R knockout TM cells. Furthermore, FLU demonstrated its protective effects by increasing the production of nitric oxide and facilitating the degradation of the extracellular matrix through the elevation of cathepsin K. These findings suggest that the S1R could be a novel target for the development of anti-fibrotic drugs and offer a new therapeutic approach for glaucoma.

Indexed as

GlaucomaGlaucoma, Open-AngleActinsAnimalsCells, CulturedFibrosisFluvoxamineHumansIntraocular PressureMiceSigma-1 ReceptorTrabecular MeshworkActinsFluvoxamineSigma-1 ReceptorfibrosisfluvoxaminePDGFsigma-1 receptortrabecular meshwork

Identifiers

PMID37511406
PMCPMC10380218
OpenAlexW4384829943

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.