Evidence mapPaperPMID 36835102Full record

ArticleInternational journal of molecular sciences2023

VDAC1 Knockout Affects Mitochondrial Oxygen Consumption Triggering a Rearrangement of ETC by Impacting on Complex I Activity.

Andrea Magrì, Salvatore Antonio Maria Cubisino, Giuseppe Battiato, Cristiana Lucia Rita Lipari, Stefano Conti Nibali, Miriam Wissam Saab, Alessandra Pittalà, Angela Maria Amorini, Vito De Pinto, Angela Messina

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

7 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Special Issue "Mitochondrial Respiration in Physiology and Pathology".International journal of molecular sciences · 2024
    Article
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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 1 institution in 1 country.

Andrea MagrìDepartment of Biological, Geological and Environmental Sciences, University of Catania, Via S. Sofia 64, 95125 Catania, Italy.ORCID 0000-0002-3080-2667
Salvatore Antonio Maria CubisinoDepartment of Biomedical and Biotechnological Sciences, University of Catania, Via S. Sofia 64, 95125 Catania, Italy.
Giuseppe BattiatoDepartment of Biomedical and Biotechnological Sciences, University of Catania, Via S. Sofia 64, 95125 Catania, Italy.
Cristiana Lucia Rita LipariDepartment of Biomedical and Biotechnological Sciences, University of Catania, Via S. Sofia 64, 95125 Catania, Italy.
Stefano Conti NibaliDepartment of Biomedical and Biotechnological Sciences, University of Catania, Via S. Sofia 64, 95125 Catania, Italy.
Miriam Wissam SaabDepartment of Biomedical and Biotechnological Sciences, Division of Medical Biochemistry, University of Catania, Via S. Sofia 97, 95123 Catania, Italy.
Alessandra PittalàDepartment of Biomedical and Biotechnological Sciences, Division of Medical Biochemistry, University of Catania, Via S. Sofia 97, 95123 Catania, Italy.
Angela Maria AmoriniDepartment of Biomedical and Biotechnological Sciences, Division of Medical Biochemistry, University of Catania, Via S. Sofia 97, 95123 Catania, Italy.ORCID 0000-0003-3525-9955
Vito De Pintowe.MitoBiotech S.R.L., C.so Italia 174, 95125 Catania, Italy.ORCID 0000-0001-5513-2906
Angela MessinaDepartment of Biological, Geological and Environmental Sciences, University of Catania, Via S. Sofia 64, 95125 Catania, Italy.ORCID 0000-0002-5745-9846
University of Catania · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Voltage-Dependent Anion-selective Channel isoform 1 (VDAC1) is the most abundant isoform of the outer mitochondrial membrane (OMM) porins and the principal gate for ions and metabolites to and from the organelle. VDAC1 is also involved in a number of additional functions, such as the regulation of apoptosis. Although the protein is not directly involved in mitochondrial respiration, its deletion in yeast triggers a complete rewiring of the whole cell metabolism, with the inactivation of the main mitochondrial functions. In this work, we analyzed in detail the impact of VDAC1 knockout on mitochondrial respiration in the near-haploid human cell line HAP1. Results indicate that, despite the presence of other VDAC isoforms in the cell, the inactivation of VDAC1 correlates with a dramatic impairment in oxygen consumption and a re-organization of the relative contributions of the electron transport chain (ETC) enzymes. Precisely, in VDAC1 knockout HAP1 cells, the complex I-linked respiration (N-pathway) is increased by drawing resources from respiratory reserves. Overall, the data reported here strengthen the key role of VDAC1 as a general regulator of mitochondrial metabolism.

Indexed as

Electron Transport Complex IMitochondriaOxygen ConsumptionVoltage-Dependent Anion Channel 1HumansMitochondrial MembranesPorinsProtein IsoformsSaccharomyces cerevisiaeElectron Transport Complex IPorinsProtein IsoformsVDAC1 protein, humanVoltage-Dependent Anion Channel 1complex IHAP1 cellsmitochondriarespiratory reserve(s)VDAC1 knockout

Identifiers

PMID36835102
PMCPMC9963415
OpenAlexW4320493468

What Socratic holds

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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 Socratic graph.