Evidence map›Paper›PMID 39765697›Full record

ReviewBiology2024

Retinal Inflammation and Reactive Müller Cells: Neurotrophins' Release and Neuroprotective Strategies.

Bijorn Omar Balzamino, Andrea Cacciamani, Lucia Dinice, Michela Cecere, Francesca Romana Pesci, Guido Ripandelli, Alessandra Micera

Abstract readReview
In one paragraph

Review in Biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

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

16 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Neuroprotective effects ofFrontiers in molecular biosciences · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Single-Cell Transcriptomics onBiomedicines · 2025
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
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

7 authors.

Bijorn Omar BalzaminoResearch and Development Laboratory for Biochemical, Molecular and Cellular Applications in Ophthalmological Science, IRCCS-Fondazione Bietti, via di Santo Stefano Rotondo 6, 00184 Rome, Italy.ORCID 0000-0002-2254-1647
Andrea CacciamaniSurgical Retina Research Unit, IRCCS-Fondazione Bietti, via di Santo Stefano Rotondo 6, 00184 Rome, Italy.ORCID 0000-0003-1793-9842
Lucia DiniceResearch and Development Laboratory for Biochemical, Molecular and Cellular Applications in Ophthalmological Science, IRCCS-Fondazione Bietti, via di Santo Stefano Rotondo 6, 00184 Rome, Italy.ORCID 0000-0002-1158-0659
Michela CecereSurgical Retina Research Unit, IRCCS-Fondazione Bietti, via di Santo Stefano Rotondo 6, 00184 Rome, Italy.ORCID 0000-0002-4614-2085
Francesca Romana PesciSurgical Retina Research Unit, IRCCS-Fondazione Bietti, via di Santo Stefano Rotondo 6, 00184 Rome, Italy.
Guido RipandelliSurgical Retina Research Unit, IRCCS-Fondazione Bietti, via di Santo Stefano Rotondo 6, 00184 Rome, Italy.ORCID 0000-0003-1119-2645
Alessandra MiceraResearch and Development Laboratory for Biochemical, Molecular and Cellular Applications in Ophthalmological Science, IRCCS-Fondazione Bietti, via di Santo Stefano Rotondo 6, 00184 Rome, Italy.ORCID 0000-0002-9375-6071

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Millions of people worldwide suffer from retinal disorders. Retinal diseases require prompt attention to restore function or reduce progressive impairments. Genetics, epigenetics, life-styling/quality and external environmental factors may contribute to developing retinal diseases. In the physiological retina, some glial cell types sustain neuron activities by guaranteeing ion homeostasis and allowing effective interaction in synaptic transmission. Upon insults, glial cells interact with neuronal and the other non-neuronal retinal cells, at least in part counteracting the biomolecular changes that may trigger retinal complications and vision loss. Several epigenetic and oxidative stress mechanisms are quickly activated to release factors that in concert with growth, fibrogenic and angiogenic factors can influence the overall microenvironment and cell-to-cell response. Reactive Müller cells participate by secreting neurotrophic/growth/angiogenic factors, cytokines/chemokines, cytotoxic/stress molecules and neurogenic inflammation peptides. Any attempt to maintain/restore the physiological condition can be interrupted by perpetuating insults, vascular dysfunction and neurodegeneration. Herein, we critically revise the current knowledge on the cell-to-cell and cell-to-mediator interplay between Müller cells, astrocytes and microglia, with respect to pro-con modulators and neuroprotective/detrimental activities, as observed by using experimental models or analyzing ocular fluids, altogether contributing a new point of view to the field of research on precision medicine.

Indexed as

agingMüller cellsNGFprecision medicineretinal disorders

Identifiers

PMID39765697
PMCPMC11673524

What Socratic 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 Socratic graph.