Evidence map›Paper›PMID 37240666›Full record

ArticleJournal of clinical medicine2023

Mitochondrial Aconitase Enzymatic Activity: A Potential Long-Term Survival Biomarker in the Blood of ALS Patients.

Cristina González-Mingot, Francisco Javier Miana-Mena, Pedro José Iñarrea, Cristina Iñiguez, José Luis Capablo, Rosario Osta, Anna Gil-Sánchez, Luis Brieva, Pilar Larrodé

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of clinical medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Inhibition of Rho-Associated Kinases ROCK1 and ROCK2 as a Therapeutic Strategy to Reactivate the RepressedThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
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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

9 authors at 5 institutions in 1 country.

Cristina González-MingotNeurology-Department, Hospital Arnau de Vilanova of Lleida, 25198 Lleida, Spain.
Francisco Javier Miana-MenaLAGENBIO-Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Aragon Institute for Health Research (IIS Aragon), Zaragoza University, 50013 Zaragoza, Spain.
Pedro José IñarreaBiochemical-Department of Biology-Faculty, Zaragoza University, 50009 Zaragoza, Spain.
Cristina IñiguezNeurology-Department, Hospital Clínico Universitario Lozano Blesa of Zaragoza, 50009 Zaragoza, Spain.
José Luis CapabloNeurology-Department, Hospital Universitario Miguel Servet of Zaragoza, 50009 Zaragoza, Spain.
Rosario OstaLAGENBIO-Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Aragon Institute for Health Research (IIS Aragon), Zaragoza University, 50013 Zaragoza, Spain.
Anna Gil-SánchezNeurology-Department, Hospital Arnau de Vilanova of Lleida, 25198 Lleida, Spain.
Luis BrievaNeurology-Department, Hospital Arnau de Vilanova of Lleida, 25198 Lleida, Spain.
Pilar LarrodéNeurology-Department, Hospital Clínico Universitario Lozano Blesa of Zaragoza, 50009 Zaragoza, Spain.
Hospital Arnau de Vilanova · ESCentro de Investigación Biomédica en Red · ESHospital Clínico Universitario Lozano Blesa · ESHospital Universitario Miguel Servet · ESUniversidad de Zaragoza · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAmyotrophic lateral sclerosis (ALS) is a multisystemic, progressive, neurodegenerative disorder. Despite it being generally fatal within a period of 2-4 years, it is highly heterogeneous; as a result, survival periods may vary greatly among individual patients. Biomarkers can serve as tools for diagnosis, prognosis, indicators of therapeutic response, and future therapeutics. Free-radical-dependent mitochondrial damage is believed to play a crucial role in neurodegeneration in ALS. Mitochondrial aconitase, which is also known as aconitase 2 (Aco2), is a key Krebs cycle enzyme and is involved in the regulation of cellular metabolism and iron homeostasis. Aco2 is very sensitive to oxidative inactivation and can aggregate and accumulate in the mitochondrial matrix, causing mitochondrial dysfunction. Loss of Aco2 activity may therefore reflect increased levels of mitochondrial dysfunction due to oxidative damage and could be relevant to ALS pathogenesis. The aim of our study was to confirm changes in mitochondrial aconitase activity in peripheral blood and to determine whether such changes are dependent on, or independent of, the patient's condition and to propose the feasibility of using them as possible valid biomarkers to quantify the progression of the disease and as a predictor of individual prognosis in ALS.

methodsWe measured the Aco2 enzymatic activity in the platelets of blood samples taken from 22 controls and 26 ALS patients at different stages of disease development. We then correlated antioxidant activity with clinical and prognostic variables.

resultsAco2 activity was significantly lower in the 26 ALS patients than in the 22 controls (

conclusionsAco2 activity seems to be an independent factor that could be used in the long-term survival prognosis of ALS. Our findings suggest that blood Aco2 could be a leading candidate for use as a biomarker to improve prognosis. More studies are needed to confirm these results.

Indexed as

aconitaseALSbiomarkerenzymatic activitymitochondrial antioxidant activity

Identifiers

PMID37240666
PMCPMC10219422
OpenAlexW4377091438

What OpenQuestion holds

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LicenceCC BY
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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.