ArticlePloS one2017
Myeloid-specific deletion of NOX2 prevents the metabolic and neurologic consequences of high fat diet.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 29 citations in OpenAlex.
- Sex-Specific Cardiovascular Protection in Developing Metabolic Syndrome: The Role of AMPK.Antioxidants (Basel, Switzerland) · 2025Article
- TBC1D1 is an energy-responsive polarization regulator of macrophages via governing ROS production in obesity.Science China. Life sciences · 2024Article
- Effect of high-fat diet on cerebral pathological changes of cerebral small vessel disease in SHR/SP rats.GeroScience · 2024Article
- Interaction of high-fat diet and brain trauma alters adipose tissue macrophages and brain microglia associated with exacerbated cognitive dysfunction.Journal of neuroinflammation · 2024Article
- NADPH oxidase exerts a B cell-intrinsic contribution to lupus risk by modulating endosomal TLR signals.The Journal of experimental medicine · 2024Article
- Mitochondrial transfer in hematological malignancies.Biomarker research · 2023Review
- Cross-Talk of NADPH Oxidases and Inflammation in Obesity.Antioxidants (Basel, Switzerland) · 2023Review
- Current Status of Obesity: Protective Role of Catechins.Antioxidants (Basel, Switzerland) · 2023Review
- Diet-induced obesity worsens allergen-induced type 2/type 17 inflammation in airways by enhancing DUOX1 activation.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Adipose tissue macrophages as potential targets for obesity and metabolic diseases.Frontiers in immunology · 2023Review
- NADPH Oxidases in Aortic Aneurysms.Antioxidants (Basel, Switzerland) · 2022Review
- The Interplay Between Adipose Tissue and Vasculature: Role of Oxidative Stress in Obesity.Frontiers in cardiovascular medicine · 2021Review
- The Emerging Roles of Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 in Skeletal Muscle Redox Signaling and Metabolism.Antioxidants & redox signaling · 2019Review
- The Role of NADPH Oxidases in the Etiology of Obesity and Metabolic Syndrome: Contribution of Individual Isoforms and Cell Biology.Antioxidants & redox signaling · 2019Review
- Estradiol and NADPH oxidase crosstalk regulates responses to high fat feeding in female mice.Experimental biology and medicine (Maywood, N.J.) · 2019Article
- IL-1 beta-mediated macrophage-hepatocyte crosstalk upregulates hepcidin under physiological low oxygen levels.Redox biology · 2019Article
- Adipose oxidative stress and protein carbonylation.The Journal of biological chemistry · 2019Review
- Nicotinamide adenine dinucleotide phosphate (reduced) oxidase 2 modulates inflammatory vigor during nonalcoholic fatty liver disease progression in mice.Hepatology communications · 2018Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
High fat diet-induced obesity is associated with inflammatory and oxidative signaling in macrophages that likely participates in metabolic and physiologic impairment. One key factor that could drive pathologic changes in macrophages is the pro-inflammatory, pro-oxidant enzyme NADPH oxidase. However, NADPH oxidase is a pleiotropic enzyme with both pathologic and physiologic functions, ruling out indiscriminant NADPH oxidase inhibition as a viable therapy. To determine if targeted inhibition of monocyte/macrophage NADPH oxidase could mitigate obesity pathology, we generated mice that lack the NADPH oxidase catalytic subunit NOX2 in myeloid lineage cells. C57Bl/6 control (NOX2-FL) and myeloid-deficient NOX2 (mNOX2-KO) mice were given high fat diet for 16 weeks, and subject to comprehensive metabolic, behavioral, and biochemical analyses. Data show that mNOX2-KO mice had lower body weight, delayed adiposity, attenuated visceral inflammation, and decreased macrophage infiltration and cell injury in visceral adipose relative to control NOX2-FL mice. Moreover, the effects of high fat diet on glucose regulation and circulating lipids were attenuated in mNOX2-KO mice. Finally, memory was impaired and markers of brain injury increased in NOX2-FL, but not mNOX2-KO mice. Collectively, these data indicate that NOX2 signaling in macrophages participates in the pathogenesis of obesity, and reinforce a key role for macrophage inflammation in diet-induced metabolic and neurologic decline. Development of macrophage/immune-specific NOX-based therapies could thus potentially be used to preserve metabolic and neurologic function in the context of obesity.
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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.