ArticleScientific reports2016
Accumulation of isolevuglandin-modified protein in normal and fibrotic lung.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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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
19 citing papers in PubMed, 27 citations in OpenAlex.
- Myocardial ferroptosis may exacerbate the progression of atrial fibrillation through isolevuglandins.European journal of medical research · 2025Review
- Epigenetic Regulation of Innate and Adaptive Immune Cells in Salt-Sensitive Hypertension.Circulation research · 2025Review
- LNK/SH2B3 loss of function increases susceptibility to murine and human atrial fibrillation.Cardiovascular research · 2024Article
- Review
- Prediction and analysis of genetic effect in idiopathic pulmonary fibrosis and gastroesophageal reflux disease.IET systems biology · 2023Article
- Mitochondrial Isolevuglandins Contribute to Vascular Oxidative Stress and Mitochondria-Targeted Scavenger of Isolevuglandins Reduces Mitochondrial Dysfunction and Hypertension.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Chromatin as a key consumer in the metabolite economy.Nature chemical biology · 2020Review
- Highly Reactive Isolevuglandins Promote Atrial Fibrillation Caused by Hypertension.JACC. Basic to translational science · 2020Article
- Isolevuglandins as mediators of disease and the development of dicarbonyl scavengers as pharmaceutical interventions.Pharmacology & therapeutics · 2020Review
- Advances in Cardiovascular Disease Lipid Research Can Provide Novel Insights Into Mycobacterial Pathogenesis.Frontiers in cellular and infection microbiology · 2019Review
- Article
- Isolevuglandins and cardiovascular disease.Prostaglandins & other lipid mediators · 2018Review
- The Role of Nrf2 in the Response to Normal Tissue Radiation Injury.Radiation research · 2018Review
- Loss of Nrf2 promotes alveolar type 2 cell loss in irradiated, fibrotic lung.Free radical biology & medicine · 2017Article
- Mechanisms of Normal Tissue Injury From Irradiation.Seminars in radiation oncology · 2017Review
- Radiation-Induced Fibrosis: Mechanisms and Opportunities to Mitigate. Report of an NCI Workshop, September 19, 2016.Radiation research · 2017Article
- Isolevuglandins as a gauge of lipid peroxidation in human tumors.Free radical biology & medicine · 2017Article
- Gene expression profiles among murine strains segregate with distinct differences in the progression of radiation-induced lung disease.Disease models & mechanisms · 2017Article
- Histone Adduction and Its Functional Impact on Epigenetics.Chemical research in toxicology · 2017Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
Protein lysine modification by γ-ketoaldehyde isomers derived from arachidonic acid, termed isolevuglandins (IsoLGs), is emerging as a mechanistic link between pathogenic reactive oxygen species and disease progression. However, the questions of whether covalent modification of proteins by IsoLGs are subject to genetic regulation and the identity of IsoLG-modified proteins remain unclear. Herein we show that Nrf2 and Nox2 are key regulators of IsoLG modification in pulmonary tissue and report on the identity of proteins analyzed by LC-MS following immunoaffinity purification of IsoLG-modified proteins. Gene ontology analysis revealed that proteins in numerous cellular pathways are susceptible to IsoLG modification. Although cells tolerate basal levels of modification, exceeding them induces apoptosis. We found prominent modification in a murine model of radiation-induced pulmonary fibrosis and in idiopathic pulmonary fibrosis, two diseases considered to be promoted by gene-regulated oxidant stress. Based on these results we hypothesize that IsoLG modification is a hitherto unrecognized sequelae that contributes to radiation-induced pulmonary injury and IPF.
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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.