Evidence map›Paper›PMID 36225228›Full record

ReviewFrontiers in neuroanatomy2022

Cellular and molecular alterations in neurons and glial cells in inherited retinal degeneration.

Natalia Martínez-Gil, Victoria Maneu, Oksana Kutsyr, Laura Fernández-Sánchez, Xavier Sánchez-Sáez, Carla Sánchez-Castillo, Laura Campello, Pedro Lax, Isabel Pinilla, Nicolás Cuenca

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neuroanatomy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

17 citing papers in PubMed, 16 citations in OpenAlex.

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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

10 authors at 3 institutions in 1 country.

Natalia Martínez-GilDepartment of Physiology, Genetics and Microbiology, University of Alicante, Alicante, Spain.
Victoria ManeuDepartment of Optics, Pharmacology and Anatomy, University of Alicante, Alicante, Spain.
Oksana KutsyrDepartment of Physiology, Genetics and Microbiology, University of Alicante, Alicante, Spain.
Laura Fernández-SánchezDepartment of Optics, Pharmacology and Anatomy, University of Alicante, Alicante, Spain.
Xavier Sánchez-SáezDepartment of Physiology, Genetics and Microbiology, University of Alicante, Alicante, Spain.
Carla Sánchez-CastilloDepartment of Physiology, Genetics and Microbiology, University of Alicante, Alicante, Spain.
Laura CampelloDepartment of Physiology, Genetics and Microbiology, University of Alicante, Alicante, Spain.
Pedro LaxDepartment of Physiology, Genetics and Microbiology, University of Alicante, Alicante, Spain.
Isabel PinillaAragón Institute for Health Research (IIS Aragón), Zaragoza, Spain.
Nicolás CuencaDepartment of Physiology, Genetics and Microbiology, University of Alicante, Alicante, Spain.
University of Alicante · ESHospital Clínico Universitario Lozano Blesa · ESInstituto de investigación sanitaria y biomédica de Alicante

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple gene mutations have been associated with inherited retinal dystrophies (IRDs). Despite the spectrum of phenotypes caused by the distinct mutations, IRDs display common physiopathology features. Cell death is accompanied by inflammation and oxidative stress. The vertebrate retina has several attributes that make this tissue vulnerable to oxidative and nitrosative imbalance. The high energy demands and active metabolism in retinal cells, as well as their continuous exposure to high oxygen levels and light-induced stress, reveal the importance of tightly regulated homeostatic processes to maintain retinal function, which are compromised in pathological conditions. In addition, the subsequent microglial activation and gliosis, which triggers the secretion of pro-inflammatory cytokines, chemokines, trophic factors, and other molecules, further worsen the degenerative process. As the disease evolves, retinal cells change their morphology and function. In disease stages where photoreceptors are lost, the remaining neurons of the retina to preserve their function seek out for new synaptic partners, which leads to a cascade of morphological alterations in retinal cells that results in a complete remodeling of the tissue. In this review, we describe important molecular and morphological changes in retinal cells that occur in response to oxidative stress and the inflammatory processes underlying IRDs.

Indexed as

cellular responsesinflammationoxidative stressreactive oxygen speciesretinal degeneration

Identifiers

PMID36225228
PMCPMC9548552
OpenAlexW4297236331

What OpenQuestion holds

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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.