ArticleJournal of vascular research2018
Absence of Nicotinamide Nucleotide Transhydrogenase in C57BL/6J Mice Exacerbates Experimental Atherosclerosis.
Article in Journal of vascular research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- Host Genetic Regulation of NLRP3 Inflammasome Cytokines Reveals Immune and Vascular Pathways in HIV.medRxiv : the preprint server for health sciences · 2026Article
- Comprehensive Proteomic Profiling Reveals Dysregulation of Angiogenesis and Inflammatory Pathways in the Brains of SIRT3 Knockout Mice.Brain sciences · 2026Article
- Potassium-Hydroxide-Based Extraction of Nicotinamide Adenine Dinucleotides from Biological Samples Offers Accurate Assessment of Intracellular Redox Status.International journal of molecular sciences · 2025Article
- Brief introduction in phenotypic and genetic differences of C57BL/6 and BALB/c mice substrains.Animal models and experimental medicine · 2025Review
- The molecular interplay among gut dysbiosis, adipose tissue, and metabolite-derived damage-associated molecular patterns in metainflammation and atherogenesis.Frontiers in immunology · 2025Review
- The C57BL/6N mouse substrain is a viable model of elastase-induced abdominal aortic aneurysm.Frontiers in cardiovascular medicine · 2024Article
- Article
- Mild Mitochondrial Uncoupling Decreases Experimental Atherosclerosis, A Proof of Concept.Journal of atherosclerosis and thrombosis · 2022Article
- Widespread discrepancy ineLife · 2022Article
- Metabolic differences and differentially expressed genes between C57BL/6J and C57BL/6N mice substrains.PloS one · 2022Article
- Inhibiting bridge integrator 2 phosphorylation leads to improved oocyte quality, ovarian health and fertility in aging and after chemotherapy in mice.Nature aging · 2021Article
- Loss ofInternational journal of molecular sciences · 2021Article
- Substrains matter in phenotyping of C57BL/6 mice.Experimental animals · 2021Review
- PCSK9 mediates the oxidative low‑density lipoprotein‑induced pyroptosis of vascular endothelial cells via the UQCRC1/ROS pathway.International journal of molecular medicine · 2021Article
- Proteomic and mitochondrial adaptations to early-life stress are distinct in juveniles and adults.Neurobiology of stress · 2020Article
- Article
- Identification of biomarkers, pathways, and potential therapeutic targets for heart failure using next-generation sequencing data and bioinformatics analysis.Therapeutic advances in cardiovascular diseaseArticle
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMitochondrial reactive oxygen species (ROS) contribute to inflammation and vascular remodeling during atherosclerotic plaque formation. C57BL/6N (6N) and C57BL/6J (6J) mice display distinct mitochondrial redox balance due to the absence of nicotinamide nucleotide transhydrogenase (NNT) in 6J mice. We hypothesize that differential NNT expression between these animals alters plaque development.
methods6N and 6J mice were treated with AAV8-PCSK9 (adeno-associated virus serotype 8/proprotein convertase subtilisin/kexin type 9) virus leading to hypercholesterolemia, increased low-density lipoprotein, and atherosclerosis in mice fed a high-fat diet (HFD). Mice were co-treated with the mitochondria-targeted superoxide dismutase mimetic MitoTEMPO to assess the contribution of mitochondrial ROS to atherosclerosis.
resultsBaseline and HFD-induced vascular superoxide is increased in 6J compared to 6N mice. MitoTEMPO diminished superoxide in both groups demonstrating differential production of mitochondrial ROS among these strains. PCSK9 treatment and HFD led to similar increases in plasma lipids in both 6N and 6J mice. However, 6J animals displayed significantly higher levels of plaque formation. MitoTEMPO reduced plasma lipids but did not affect plaque formation in 6N mice. In contrast, MitoTEMPO surprisingly increased plaque formation in 6J mice.
conclusionThese data indicate that loss of NNT increases vascular ROS production and exacerbates atherosclerotic plaque development.
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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.