Cell Motility Dynamics in Glaucoma: Mechanisms, Pathogenic Roles, and Therapeutic Targeting.

Dario Rusciano, Caterina Gagliano, Alessandro Avitabile, José Fernando Maya-Vetencourt

Abstract readReview

In one paragraph

Review in Medicina (Kaunas, Lithuania), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it

0cells of the map it votes in

0citing papers in PubMed

–field-weighted citation impact

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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Dario RuscianoFidia Pharmaceuticals, Ophthalmology Research, Catania University, 95100 Catania, Italy.ORCID 0000-0002-9577-2585

Caterina GaglianoFaculty of Medicine and Surgery, University of Enna "Kore", 94100 Enna, Italy.ORCID 0000-0001-8424-0068

Alessandro AvitabileNeurovisual Science Technology (NEST), 95100 Catania, Italy.ORCID 0009-0003-1051-876X

José Fernando Maya-VetencourtDepartment of Biology, Physiology Institute, University of Pisa, 56100 Pisa, Italy.ORCID 0000-0003-3808-8944

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell motility-the dynamic process encompassing migration, adhesion modulation, cytoskeletal remodeling, and extracellular matrix (ECM) interactions-is fundamental to ocular homeostasis. In glaucoma, disrupted motility of trabecular meshwork (TM) and Schlemm's canal (SC) cells contributes to impaired aqueous humor outflow and elevated intraocular pressure (IOP), while reactive motility of optic nerve head (ONH) glial cells promotes fibrosis and neurodegeneration. Mechanistically, TM/SC motility is regulated by Rho GTPase and ROCK signaling, focal adhesion dynamics, and ECM interactions, while glial cells respond to mechanical stress and cytokines such as TGF-β

Indexed as

Cell MovementGlaucomaAqueous HumorHumansIntraocular PressureTrabecular Meshworkastrocyte reactivitycell motilityendothelial–mesenchymal transitionmechanotransductionRho/ROCK signalingSchlemm’s canalTGF-β2trabecular meshwork

Identifiers

PMID41470223

DOI10.3390/medicina61122219

PMCPMC12734998

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Registered trials

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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.