ArticleThe Journal of biological chemistry2012
Protein carbonylation and adipocyte mitochondrial function.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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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.
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.
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Who cites it
39 citing papers in PubMed, 70 citations in OpenAlex.
- HuR-dependent expression of RyR2 contributes to calcium-mediated thermogenesis in murine brown adipocytes.Scientific reports · 2026Article
- Cadmium Toxicity Effects on Histone Modifiers, Enzyme Activity and Adipokines in Human Adipose Tissue Cells.Molecules (Basel, Switzerland) · 2026Article
- Mitochondrial Dysfunctions in Human Primary Coenzyme QBiomolecules · 2026Review
- Emerging insights into pulmonary hypertension: the potential role of mitochondrial dysfunction and redox homeostasis.Molecular and cellular biochemistry · 2025Review
- Pathophysiology and emerging biomarkers of cardiovascular-renal-hepato-metabolic syndrome.Frontiers in cardiovascular medicine · 2025Review
- Lipid peroxidation products induce carbonyl stress, mitochondrial dysfunction, and cellular senescence in human and murine cells.Aging cell · 2025Article
- Sustained caloric restriction potentiates insulin action by activating prostacyclin synthase.Obesity (Silver Spring, Md.) · 2024Article
- Adiponectin Resistance in Obesity: Adiponectin Leptin/Insulin Interaction.Advances in experimental medicine and biology · 2024Review
- ClpP/ClpX deficiency impairs mitochondrial functions and mTORC1 signaling during spermatogenesis.Communications biology · 2023Article
- Parkinson's disease neurons exhibit alterations in mitochondrial quality control proteins.NPJ Parkinson's disease · 2023Article
- Carbonylated Proteins as Key Regulators in the Progression of Metabolic Syndrome.Antioxidants (Basel, Switzerland) · 2023Article
- Differences in in vitro microglial accumulation of the energy metabolism tracers [Scientific reports · 2021Article
- Small molecule inhibitors of the mitochondrial ClpXP protease possess cytostatic potential and re-sensitize chemo-resistant cancers.Scientific reports · 2021Article
- Histone Carbonylation Is a Redox-Regulated Epigenomic Mark That Accumulates with Obesity and Aging.Antioxidants (Basel, Switzerland) · 2020Article
- Fumarate and oxidative stress synergize to promote stability of C/EBP homologous protein in the adipocyte.Free radical biology & medicine · 2020Article
- Beyond adiponectin and leptin: adipose tissue-derived mediators of inter-organ communication.Journal of lipid research · 2019Review
- Signaling and Regulation of the Mitochondrial Unfolded Protein Response.Cold Spring Harbor perspectives in biology · 2019Review
- Adipose oxidative stress and protein carbonylation.The Journal of biological chemistry · 2019Review
- Insights into the respiratory chain and oxidative stress.Bioscience reports · 2018Review
- Obesity-induced protein carbonylation in murine adipose tissue regulates the DNA-binding domain of nuclear zinc finger proteins.The Journal of biological chemistry · 2018Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
Carbonylation is the covalent, non-reversible modification of the side chains of cysteine, histidine, and lysine residues by lipid peroxidation end products such as 4-hydroxy- and 4-oxononenal. In adipose tissue the effects of such modifications are associated with increased oxidative stress and metabolic dysregulation centered on mitochondrial energy metabolism. To address the role of protein carbonylation in the pathogenesis of mitochondrial dysfunction, quantitative proteomics was employed to identify specific targets of carbonylation in GSTA4-silenced or overexpressing 3T3-L1 adipocytes. GSTA4-silenced adipocytes displayed elevated carbonylation of several key mitochondrial proteins including the phosphate carrier protein, NADH dehydrogenase 1α subcomplexes 2 and 3, translocase of inner mitochondrial membrane 50, and valyl-tRNA synthetase. Elevated protein carbonylation is accompanied by diminished complex I activity, impaired respiration, increased superoxide production, and a reduction in membrane potential without changes in mitochondrial number, area, or density. Silencing of the phosphate carrier or NADH dehydrogenase 1α subcomplexes 2 or 3 in 3T3-L1 cells results in decreased basal and maximal respiration. These results suggest that protein carbonylation plays a major instigating role in cytokine-dependent mitochondrial dysfunction and may be linked to the development of insulin resistance in the adipocyte.
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Registered trials
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.