ArticleJournal of hypertension2012
Novel genes as primary triggers for polygenic hypertension.
Article in Journal of hypertension, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 17 citations in OpenAlex.
- Effect of Cardiotonic Steroid Marinobufagenin on Vascular Remodeling and Cognitive Impairment in Young Dahl-S Rats.International journal of molecular sciences · 2022Article
- Deep transcriptomic profiling of Dahl salt-sensitive rat kidneys with mutant form of Resp18.Biochemical and biophysical research communications · 2021Article
- Conserved mammalian modularity of quantitative trait loci revealed human functional orthologs in blood pressure control.PloS one · 2020Article
- Monoclonal Antibody to Marinobufagenin Downregulates TGFβ Profibrotic Signaling in Left Ventricle and Kidney and Reduces Tissue Remodeling in Salt-Sensitive Hypertension.Journal of the American Heart Association · 2019Article
- Dr Lewis Kitchener Dahl, the Dahl rats, and the "inconvenient truth" about the genetics of hypertension.Hypertension (Dallas, Tex. : 1979) · 2015Article
- Application of quantitative trait locus mapping and transcriptomics to studies of the senescence-accelerated phenotype in rats.BMC genomics · 2014Article
- Myotubularin-related protein 4 (MTMR4) attenuates BMP/Dpp signaling by dephosphorylation of Smad proteins.The Journal of biological chemistry · 2013Article
- Essential hypertension: perspectives and future directions.Journal of hypertension · 2012Article
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7 authors at 3 institutions in 3 countries.
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Abstract
objectivesThe discovery of causative genes leading to hypertension in animal models can reveal new mechanistic insights into blood pressure (BP) regulations. Previously, we isolated segments that harbor BP quantitative trait loci (QTLs) on rat chromosome 10 as defined by congenic strains made from crosses of inbred hypertensive Dahl salt-sensitive (DSS) and normotensive Lewis rats. The aim of the current study was to identify hypertension-causing genes for each QTL.
methodsMolecular analysis was performed.
resultsA systematic and comprehensive molecular analysis divulged particular genes that carry nonconserved mutations. Specifically, the proline rich 11 gene is likely responsible for C10QTL5. C10QTL1 is one of five genes, namely Benzodiazepine receptor associated protein 1, Loc689764, myotubularin related protein 4, protein phosphatase 1E, PP2C domain containing and ring finger protein 43. Loc100363423 with no known function is a candidate for C10QTL3. The ATP-binding cassette, subfamily A (ABC1), member 8a gene is probably responsible for C10QTL2.
conclusionsPrimary genes initiating polygenic hypertension are those not known to be involved in BP modulation. Novel pathways towards BP homeostasis appear to underlie the functionality of C10QTL5, C10QTL1 and C10QTL3 and C10QTL2. Moreover, these genes may become innovative targets for the diagnosis and therapeutics of essential hypertension.
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