Evidence map›Paper›PMID 35221932›Full record

ArticleFrontiers in neuroanatomy2022

Programmed Cell Death and Autophagy in an

Kevin Puertas-Neyra, Nadia Galindo-Cabello, Leticia A Hernández-Rodríguez, Fernando González-Pérez, José Carlos Rodríguez-Cabello, Rogelio González-Sarmiento, José Carlos Pastor, Ricardo Usategui-Martín, Ivan Fernandez-Bueno

Open access · goldAbstract read
In one paragraph

Article 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 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. 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 4 institutions in 2 countries.

Kevin Puertas-NeyraRetina Group, Instituto Universitario de Oftalmobiología Aplicada (IOBA), Universidad de Valladolid, Valladolid, Spain.
Nadia Galindo-CabelloRetina Group, Instituto Universitario de Oftalmobiología Aplicada (IOBA), Universidad de Valladolid, Valladolid, Spain.
Leticia A Hernández-RodríguezRetina Group, Instituto Universitario de Oftalmobiología Aplicada (IOBA), Universidad de Valladolid, Valladolid, Spain.
Fernando González-PérezGroup for Advanced Materials and Nanobiotechnology (GIR BIOFORGE), CIBER-BBN, Edificio LUCIA, Universidad de Valladolid, Valladolid, Spain.
José Carlos Rodríguez-CabelloGroup for Advanced Materials and Nanobiotechnology (GIR BIOFORGE), CIBER-BBN, Edificio LUCIA, Universidad de Valladolid, Valladolid, Spain.
Rogelio González-SarmientoMolecular Medicine Unit, Department of Medicine, University of Salamanca, Salamanca, Spain.
José Carlos PastorRetina Group, Instituto Universitario de Oftalmobiología Aplicada (IOBA), Universidad de Valladolid, Valladolid, Spain.
Ricardo Usategui-MartínRetina Group, Instituto Universitario de Oftalmobiología Aplicada (IOBA), Universidad de Valladolid, Valladolid, Spain.
Ivan Fernandez-BuenoRetina Group, Instituto Universitario de Oftalmobiología Aplicada (IOBA), Universidad de Valladolid, Valladolid, Spain.
Universidad de Valladolid · ESJunta de Castilla y León · ESCentro de Investigación del Cáncer · ESMinisterio de Ciencia, Innovación y Universidades

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retinal neurodegenerative diseases are the leading causes of visual impairment and irreversible blindness worldwide. Although the retinal response to injury remains closely similar between different retinal neurodegenerative diseases, available therapeutic alternatives are only palliative, too expensive, or very specific, such as gene therapy. In that sense, the development of broad-spectrum neuroprotective therapies seems to be an excellent option. In this regard, it is essential to identify molecular targets involved in retinal degeneration, such as cell death mechanisms. Apoptosis has been considered as the primary cell death mechanism during retinal degeneration; however, recent studies have demonstrated that the only use of anti-apoptotic drugs is not enough to confer good neuroprotection in terms of cell viability and preservation. For that reason, the interrelationship that exists between apoptosis and other cell death mechanisms needs to be characterized deeply to design future therapeutic options that simultaneously block the main cell death pathways. In that sense, the study aimed to characterize the programmed cell death (in terms of apoptosis and necroptosis) and autophagy response and modulation in retinal neurodegenerative diseases, using an

Indexed as

apoptosisautophagynecroptosisneurodegenerationretina

Identifiers

PMID35221932
PMCPMC8873173
OpenAlexW4210997452

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.