ArticleHypertension (Dallas, Tex. : 1979)2018
Susceptibility to Hypertensive Renal Disease in the Spontaneously Hypertensive Rat Is Influenced by 2 Loci Affecting Blood Pressure and Immunoglobulin Repertoire.
Article in Hypertension (Dallas, Tex. : 1979), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 18 citations in OpenAlex.
- Polygenic genetic variation affecting antibody formation underlies hypertensive renal injury in the stroke-prone spontaneously hypertensive rat.American journal of physiology. Renal physiology · 2023Article
- Sex- and age-related differences in renal and cardiac injury and senescence in stroke-prone spontaneously hypertensive rats.Biology of sex differences · 2023Article
- mRatBN7.2: familiar and unfamiliar features of a new rat genome reference assembly.Physiological genomics · 2022Review
- 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
- Genetic Susceptibility to Hypertension-Induced Renal Injury.Hypertension (Dallas, Tex. : 1979) · 2018Article
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8 authors at 1 institution in 1 country.
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Abstract
High blood pressure exerts its deleterious effects on health largely through acceleration of end-organ diseases. Among these, progressive loss of renal function is particularly important, not only for the direct consequences of kidney damage but also because loss of renal function is associated with amplification of other adverse cardiovascular outcomes. Genetic susceptibility to hypertension and associated end-organ disease is non-Mendelian in both humans and in a rodent model, the spontaneously hypertensive rat (SHR). Here, we report that hypertensive end-organ disease in the inbred SHR-A3 line is attributable to genetic variation in the immunoglobulin heavy chain on chromosome 6. This variation coexists with variation in a 10 Mb block on chromosome 17 that contains genetic variation in 2 genes involved in immunoglobulin Fc receptor signaling. Substitution of these genomic regions into the SHR-A3 genome from the closely related, but injury-resistant, SHR-B2 line normalizes both biomarker and histological measures of renal injury. Our findings indicate that genetic variation leads to a contribution by immune mechanisms hypertensive end-organ injury and that, in this rat model, disease is influenced by differences in germ line antibody repertoire.
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