ArticleJournal of the American Heart Association2016
Ndufc2 Gene Inhibition Is Associated With Mitochondrial Dysfunction and Increased Stroke Susceptibility in an Animal Model of Complex Human Disease.
Article in Journal of the American Heart Association, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 78 citations in OpenAlex.
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- Mitochondrial Dysfunction in the Cardiovascular Disease Continuum: Problems of Studying the Progression During the Follow-Up of the Pathologies.International journal of molecular sciences · 2025Review
- Cardioprotective Potential of ApoE-Derived Peptide (ApoEFrag) in Myocardial Infarction in Rats: A Mechanistic Study.ACS pharmacology & translational science · 2025Article
- Early and late gut microbiota signatures of stroke in high salt-fed stroke-prone spontaneously hypertensive rats.Scientific reports · 2024Article
- Cis-eQTLs in seven duck tissues identify novel candidate genes for growth and carcass traits.BMC genomics · 2024Article
- Role of autophagy in ischemic stroke: insights from animal models and preliminary evidence in the human disease.Frontiers in cell and developmental biology · 2024Review
- Polymorphic variants at NDUFC2, encoding a mitochondrial complex I subunit, associate with cardiac hypertrophy in human hypertension.Molecular medicine (Cambridge, Mass.) · 2023Article
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- Genetic Modifications to Alter Blood Pressure Level.Biomedicines · 2022Review
- Multiple Myeloma-Derived Extracellular Vesicles Modulate the Bone Marrow Immune Microenvironment.Frontiers in immunology · 2022Article
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- Differential Expression of Sphingolipid Metabolizing Enzymes in Spontaneously Hypertensive Rats: A Possible Substrate for Susceptibility to Brain and Kidney Damage.International journal of molecular sciences · 2021Article
- An Integrative Transcriptome-Wide Analysis of Amyotrophic Lateral Sclerosis for the Identification of Potential Genetic Markers and Drug Candidates.International journal of molecular sciences · 2021Article
- The Mysterious Multitude: Structural Perspective on the Accessory Subunits of Respiratory Complex I.Frontiers in molecular biosciences · 2021Review
- Rat models of human diseases and related phenotypes: a systematic inventory of the causative genes.Journal of biomedical science · 2020Review
- Pharmacological restoration of autophagy reduces hypertension-related stroke occurrence.Autophagy · 2020Article
- Brain Overexpression of Uncoupling Protein-2 (UCP2) Delays Renal Damage and Stroke Occurrence in Stroke-Prone Spontaneously Hypertensive Rats.International journal of molecular sciences · 2020Article
- Review
- High-Throughput RNA Sequencing RevealsGenes · 2019Article
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Authors and funding
22 authors at 8 institutions in 3 countries.
Funding
Abstract
backgroundThe genetic basis of stroke susceptibility remains to be elucidated. STR1 quantitative trait locus (STR1/QTL) was identified on rat chromosome 1 of stroke-prone spontaneously hypertensive rat (SHRSP) upon Japanese-style stroke-permissive diet (JD), and it contributes to 20% of the stroke phenotype variance. METHODS AND
resultsNine hundred eighty-six probe sets mapping on STR1 were selected from the Rat RAE230A array and screened through a microarray differential expression analysis in brains of SHRSP and stroke-resistant SHR (SHRSR) fed with either regular diet or JD. The gene encoding Ndufc2 (NADH dehydrogenase [ubiquinone] 1 subunit), mapping 8 Mb apart from STR1/QTL Lod score peak, was found significantly down-regulated under JD in SHRSP compared to SHRSR. Ndufc2 disruption altered complex I assembly and activity, reduced mitochondrial membrane potential and ATP levels, and increased reactive oxygen species production and inflammation both in vitro and in vivo. SHRSR carrying heterozygous Ndufc2 deletion showed renal abnormalities and stroke occurrence under JD, similarly to SHRSP. In humans, T allele variant at NDUFC2/rs11237379 was associated with significant reduction in gene expression and with increased occurrence of early-onset ischemic stroke by recessive mode of transmission (odds ratio [OR], 1.39; CI, 1.07-1.80; P=0.012). Subjects carrying TT/rs11237379 and A allele variant at NDUFC2/rs641836 had further increased risk of stroke (OR=1.56; CI, 1.14-2.13; P=0.006).
conclusionsA significant reduction of Ndufc2 expression causes complex I dysfunction and contributes to stroke susceptibility in SHRSP. Moreover, our current evidence may suggest that Ndufc2 can contribute to an increased occurrence of early-onset ischemic stroke in humans.
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