ArticleCirculation. Cardiovascular genetics2011
High-resolution identity by descent mapping uncovers the genetic basis for blood pressure differences between spontaneously hypertensive rat lines.
Article in Circulation. Cardiovascular genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 29 citations in OpenAlex.
- T-cells regulate albuminuria but not hypertension, renal histology, or the medullary transcriptome in the Dahl SSCD247American journal of physiology. Renal physiology · 2024Article
- Polygenic genetic variation affecting antibody formation underlies hypertensive renal injury in the stroke-prone spontaneously hypertensive rat.American journal of physiology. Renal physiology · 2023Article
- Whole genome sequence analysis of apparent treatment resistant hypertension status in participants from the Trans-Omics for Precision Medicine program.Frontiers in genetics · 2023Article
- Emerging Insights Into Chronic Renal Disease Pathogenesis in Hypertension From Human and Animal Genomic Studies.Hypertension (Dallas, Tex. : 1979) · 2021Review
- Genetic susceptibility of hypertension-induced kidney disease.Physiological reports · 2021Review
- Natural genetic variation in Stim1 creates stroke in the spontaneously hypertensive rat.Genes and immunity · 2020Article
- Article
- Germ-line genetic variation in the immunoglobulin heavy chain creates stroke susceptibility in the spontaneously hypertensive rat.Physiological genomics · 2019Article
- Adaptive Immunity in Hypertension.Current hypertension reports · 2019Review
- Susceptibility to Hypertensive Renal Disease in the Spontaneously Hypertensive Rat Is Influenced by 2 Loci Affecting Blood Pressure and Immunoglobulin Repertoire.Hypertension (Dallas, Tex. : 1979) · 2018Article
- Genetic Susceptibility to Hypertension-Induced Renal Injury.Hypertension (Dallas, Tex. : 1979) · 2018Article
- Inter-individual variation in adaptations to endurance and resistance exercise training: genetic approaches towards understanding a complex phenotype.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Genetics of hypertension: an assessment of progress in the spontaneously hypertensive rat.Physiological genomics · 2017Review
- Renal inflammation and injury are associated with lymphangiogenesis in hypertension.American journal of physiology. Renal physiology · 2017Article
- Mycophenolate mofetil prevents cerebrovascular injury in stroke-prone spontaneously hypertensive rats.Physiological genomics · 2017Article
- Defective Store-Operated Calcium Entry Causes Partial Nephrogenic Diabetes Insipidus.Journal of the American Society of Nephrology : JASN · 2016Article
- Hypertensive renal injury is associated with gene variation affecting immune signaling.Circulation. Cardiovascular genetics · 2014Article
- Diversity in the preimmune immunoglobulin repertoire of SHR lines susceptible and resistant to end-organ injury.Genes and immunity · 2014Article
- Genomic structure of nucleotide diversity among Lyon rat models of metabolic syndrome.BMC genomics · 2014Article
- Hypertensive renal disease: susceptibility and resistance in inbred hypertensive rat lines.Journal of hypertension · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundThe recent development of a large panel of genome-wide single nucleotide polymorphisms (SNPs) provides the opportunity to examine genetic relationships between distinct SHR lines that share hypertension but differ in their susceptibility to hypertensive end-organ disease. METHODS AND
resultsWe compared genotypes at nearly 10,000 SNPs obtained for the hypertension end-organ injury-susceptible spontaneously hypertensive rat (SHR)-A3 (SHRSP, SHR-stroke prone) line and the injury-resistant SHR-B2 line. This revealed that that the 2 lines were genetically identical by descent (IBD) across 86.6% of the genome. Areas of the genome that were not IBD were distributed across 19 of the 20 autosomes and the X chromosome. A block structure of non-IBD comprising a total of 121 haplotype blocks was formed by clustering of SNPs inherited from different ancestors. To test the null hypothesis that distinct SHR lines share a common set of hypertension susceptibility alleles, we compared blood pressure in adult SHR animals from both lines and their F1 and F2 progeny using telemetry. In 16- to 18-week-old animals fed a normal diet, systolic blood pressure (SBP, mm Hg) in SHR-A3 was 205.7 ± 3.86 (mean ± SEM, n = 26), whereas in similar SHR-B2 animals, SBP was 186.7 ± 2.53 (n = 20). In F1 and F2 animals, SBP was 188.2 ± 4.23 (n = 19) and 185.6 ± 1.1 (n = 211), respectively (P<10(-6), ANOVA). To identify non-IBD haplotype blocks contributing to blood pressure differences between these SHR lines, we developed a high-throughput SNP genotyping system to genotype SNPs marking non-IBD blocks. We mapped a single non-IBD block on chromosome 17 extending over <10 Mb, at which SHR-A3 alleles significantly elevate blood pressure compared with SHR-B2.
conclusionsThus hypertension in SHR-A3 and -B2 appears to arise from an overlapping set of susceptibility alleles, with SHR-A3 possessing an additional hypertension locus that contributes to further increase blood pressure.
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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 Socratic graph.