Evidence map›Paper›PMID 34360957›Full record

ArticleInternational journal of molecular sciences2021

Progressive Mitochondrial SOD1

Iago Méndez-López, Francisco J Sancho-Bielsa, Tobias Engel, Antonio G García, Juan Fernando Padín

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

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  12. Tubulin Acetylation and the Cellular Mechanosensing and Stress Response.Results and problems in cell differentiation · 2025
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  16. Forty years of the adrenal chromaffin cell through ISCCB meetings around the world.Pflugers Archiv : European journal of physiology · 2023
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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

5 authors at 3 institutions in 2 countries.

Iago Méndez-LópezInstituto Teófilo Hernando and Departamento de Farmacología y Terapéutica, Facultad de Medicina, Universidad Autónoma de Madrid (UAM), 28029 Madrid, Spain.ORCID 0000-0002-3428-1109
Francisco J Sancho-BielsaDepartamento de Ciencias Médicas, Facultad de Medicina, Universidad de Castilla-La Mancha (UCLM), 13005 Ciudad Real, Spain.ORCID 0000-0003-3521-5477
Tobias EngelDepartment of Physiology & Medical Physics, RCSI University of Medicine and Health Sciences, D02 YN77 Dublin, Ireland.ORCID 0000-0001-9137-0637
Antonio G GarcíaInstituto Teófilo Hernando and Departamento de Farmacología y Terapéutica, Facultad de Medicina, Universidad Autónoma de Madrid (UAM), 28029 Madrid, Spain.
Juan Fernando PadínInstituto Teófilo Hernando and Departamento de Farmacología y Terapéutica, Facultad de Medicina, Universidad Autónoma de Madrid (UAM), 28029 Madrid, Spain.
Universidad Autónoma de Madrid · ESRoyal College of Surgeons in Ireland · IEUniversity of Castilla-La Mancha · ES

Funding

Ministerio de Economía, Industria y Competitividad, Gobierno de España 2016-78892-RMinisterio de Economía, Industria y Competitividad, Gobierno de España EEBB-I-17-12697Ministerio de Economía, Industria y Competitividad, Gobierno de España EEBB-I-18-13033Ministerio de Economía, Industria y Competitividad, Gobierno de España FPI BES-2014-069005Ministerio de Economía, Industria y Competitividad, Gobierno de España SAF2013-44108-PScience Foundation Ireland 16/RC/3948Science Foundation Ireland 17/CDA/4708
6 · The paper itself

Abstract

In recent years, the "non-autonomous motor neuron death" hypothesis has become more consolidated behind amyotrophic lateral sclerosis (ALS). It postulates that cells other than motor neurons participate in the pathology. In fact, the involvement of the autonomic nervous system is fundamental since patients die of sudden death when they become unable to compensate for cardiorespiratory arrest. Mitochondria are thought to play a fundamental role in the physiopathology of ALS, as they are compromised in multiple ALS models in different cell types, and it also occurs in other neurodegenerative diseases. Our study aimed to uncover mitochondrial alterations in the sympathoadrenal system of a mouse model of ALS, from a structural, bioenergetic and functional perspective during disease instauration. We studied the adrenal chromaffin cell from mutant SOD1

Indexed as

Adrenal GlandsAmyotrophic Lateral SclerosisAnimalsCells, CulturedChromaffin CellsDown-RegulationGTP PhosphohydrolasesMembrane Potential, MitochondrialMiceMice, Inbred C57BLMitochondriaMutation, MissenseReactive Oxygen SpeciesSuperoxide Dismutase-1GTP PhosphohydrolasesOpa1 protein, mouseReactive Oxygen SpeciesSod1 protein, mouseSuperoxide Dismutase-1amyotrophic lateral sclerosischromaffin cellmitochondrial dysfunctionOPA1SOD1G93A

Identifiers

PMID34360957
PMCPMC8347639
OpenAlexW3193132492

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.