ArticleChemical research in toxicology2012
Metabolic impact of 4-hydroxynonenal on macrophage-like RAW 264.7 function and activation.
Article in Chemical research in toxicology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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.
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.
Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- SIOOTAntibiotics (Basel, Switzerland) · 2026Article
- Protection against lethal sepsis following immunization withInfection and immunity · 2023Article
- Redox Properties, Bioactivity and Health Effects of Indicaxanthin, a Bioavailable Phytochemical fromAntioxidants (Basel, Switzerland) · 2022Review
- IL-23 signaling prevents ferroptosis-driven renal immunopathology during candidiasis.Nature communications · 2022Article
- The Mito-Hormetic Mechanisms of Ozone in the Clearance of SARS-CoV2 and in the COVID-19 Therapy.Biomedicines · 2022Review
- 4-Hydroxy-Trans-2-Nonenal in the Regulation of Anti-Oxidative and Pro-Inflammatory Signaling Pathways.Oxidative medicine and cellular longevity · 2019Review
- Multianalyte Physiological Microanalytical Devices.Annual review of analytical chemistry (Palo Alto, Calif.) · 2017Review
- Signaling by 4-hydroxy-2-nonenal: Exposure protocols, target selectivity and degradation.Archives of biochemistry and biophysics · 2017Review
- Hydrogen Sulfide Donors Activated by Reactive Oxygen Species.Angewandte Chemie (International ed. in English) · 2016Article
- Pleiotropic effects of 4-hydroxynonenal on oxidative burst and phagocytosis in neutrophils.Redox biology · 2016Article
- The relevance and potential roles of microphysiological systems in biology and medicine.Experimental biology and medicine (Maywood, N.J.) · 2014Article
- Article
- Lipid peroxidation: production, metabolism, and signaling mechanisms of malondialdehyde and 4-hydroxy-2-nonenal.Oxidative medicine and cellular longevity · 2014Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Metabolic profiling of macrophage metabolic response upon exposure to 4-hydroxynonenal (HNE) demonstrates that HNE does not simply inactivate superoxide-generating enzymes but also could be responsible for the impairment of downfield signaling pathways. Multianalyte microphysiometry (MAMP) was employed to simultaneously measure perturbations in extracellular acidification, lactate production, and oxygen consumption for the examination of aerobic and anaerobic pathways. Combining the activation of oxidative burst with phorbol myristate acetate (PMA) and the immunosuppression with HNE, the complex nature of HNE toxicity was determined to be concentration- and time-dependent. Further analysis was utilized to assess the temporal effect of HNE on reactive oxygen species (ROS) production and on protein kinase C (PKC). Increased levels of HNE with decreasing PKC activity suggest that PKC is a target for HNE adductation prior to oxidative burst. Additionally, localization of PKC to the cell membrane was prevented with the introduction of HNE, demonstrating a consequence of HNE adductation on NADPH activation. The impairment of ROS by HNE suggests that HNE has a greater role in foam cell formation and tissue damage than is already known. Although work has been performed to understand the effect of HNE's regulation of specific signaling pathways, details regarding its involvement in cellular metabolism as a whole are generally unknown. This study examines the impact of HNE on macrophage oxidative burst and identifies PKC as a key protein for HNE suppression and eventual metabolic response.
Indexed as
Identifiers
What OpenQuestion holds
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.