ArticleThe Journal of clinical investigation2006
A new cardiac MASTer switch for the renin-angiotensin system.
Article in The Journal of clinical investigation, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed, 20 citations in OpenAlex.
- Classical Renin-Angiotensin system in kidney physiology.Comprehensive Physiology · 2014Review
- Direct evidence for intrarenal chymase-dependent angiotensin II formation on the diabetic renal microvasculature.Hypertension (Dallas, Tex. : 1979) · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aspartyl protease renin was first isolated from the kidney by Tigerstedt more than a century ago. In the kidney, renin secretion is tightly linked to sodium intake and renal perfusion pressure, reflecting the important role of the renin-angiotensin system (RAS) in controlling body fluid volume and blood pressure. The study by Mackins et al. in this issue of the JCI describes a novel source of renin: the mast cell (see the related article beginning on page 1063). This discovery suggests a distinct pathway for activation of the RAS that may have a particular impact on the pathogenesis of chronic tissue injury as well as more acute pathology such as arrhythmias in the heart.
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