ArticleOxidative medicine and cellular longevity2018
Increased Mitochondrial Protein Levels and Bioenergetics in the
Article in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Mitochondrial Impairment in Unloaded Postural Muscle: Mechanisms Driving Loss of Muscle Function and Mass.Antioxidants (Basel, Switzerland) · 2026Review
- Familial, constitutional, and combined idiopathic short stature: longitudinal growth patterns and pubertal effects.Frontiers in pediatrics · 2026Article
- NCells · 2024Article
- Cardiac Wolframinopathies: A Case Report of Myocarditis and a Literature Review of Cardiac Involvement in Wolfram Syndrome 1.Journal of clinical medicine · 2024Review
- Genomics of Wolfram Syndrome 1 (WFS1).Biomolecules · 2023Review
- Depletion of WFS1 compromises mitochondrial function in hiPSC-derived neuronal models of Wolfram syndrome.Stem cell reports · 2023Article
- Wolframin deficiency is accompanied with metabolic inflexibility in rat striated muscles.Biochemistry and biophysics reports · 2022Article
- Multiomic analysis on human cell model of wolfram syndrome reveals changes in mitochondrial morphology and function.Cell communication and signaling : CCS · 2021Article
- Article
- Article
- Proteomic dataset of wolframin-deficient mouse heart and skeletal muscles.Data in brief · 2018Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Wfs1 deficiency leads to a progressive loss of plasma insulin concentration, which should reduce the consumption of glucose in insulin-dependent tissues, causing a variety of changes in intracellular energy metabolism. Our objective here was to assess the changes in the amount and function of mitochondrial proteins in different muscles of Wfs1-deficient mice. Mitochondrial functions were assayed by high-resolution oxygraphy of permeabilized muscle fibers; the protein amount was evaluated by liquid chromatography tandem mass spectrometry (LC/MS/MS) analysis and mRNA levels of the uncoupler proteins UCP2 and UCP3 by real-time PCR; and citrate synthase (CS) activity was determined spectrophotometrically in muscle homogenates. Compared to controls, there were no changes in proton leak and citrate synthase activity in the heart and
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Registered trials
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