ArticleKidney & blood pressure research2016
Characterization and Activation of NLRP3 Inflammasomes in the Renal Medulla in Mice.
Article in Kidney & blood pressure research, 2016. 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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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Interaction of Angiotensin II AT1 Receptors with Purinergic P2X Receptors in Regulating Renal Afferent Arterioles in Angiotensin II-Dependent Hypertension.International journal of molecular sciences · 2023Review
- Evaluating feline lower urinary tract disease: Doppler ultrasound of the kidneys.Journal of feline medicine and surgery · 2023Article
- Role of inflammation, immunity, and oxidative stress in hypertension: New insights and potential therapeutic targets.Frontiers in immunology · 2022Review
- Release and Actions of Inflammatory Exosomes in Pulmonary Emphysema: Potential Therapeutic Target of Acupuncture.Journal of inflammation research · 2021Article
- Role of the thioredoxin interacting protein in diabetic nephropathy and the mechanism of regulating NOD‑like receptor protein 3 inflammatory corpuscle.International journal of molecular medicine · 2019Article
- Inflammation, Immunity, and Oxidative Stress in Hypertension-Partners in Crime?Advances in chronic kidney disease · 2019Review
- Sphingolipids and Redox Signaling in Renal Regulation and Chronic Kidney Diseases.Antioxidants & redox signaling · 2018Article
- Trimethylamine-N-Oxide Instigates NLRP3 Inflammasome Activation and Endothelial Dysfunction.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
BACKGROUND/
aimsRecent studies have indicated that local inflammatory mediators are importantly involved in the regulation of renal function. However, it remains unknown how such local inflammation is triggered intracellularly in the kidney. The present study was designed to characterize the inflammasome centered by Nlrp3 in the kidney and also test the effect of its activation in the renal medulla. METHODS AND
resultsBy immunohistochemistry analysis, we found that inflammasome components, Nlrp3, Asc and caspase-1, were ubiquitously distributed in different kidney areas. The caspase-1 activity and IL-1β production were particularly high in the renal outer medulla compared to other kidney regions. Further confocal microscopy and RT-PCR analysis showed that Nlrp3, Asc and caspase-1 were particularly enriched in the thick ascending limb of Henle's loop. In anesthetized mice, medullary infusion of Nlrp3 inflammasome activator, monosodium urate (MSU), induced significant decreases in sodium excretion and medullary blood flow without changes in mean arterial blood pressure and renal cortical blood flow. Caspase-1 inhibitor, Ac-YVAD-CMK and deletion of Nlrp3 or Asc gene abolished MSU-induced decreases in renal sodium excretion and MBF.
conclusionOur results indicate that renal medullary Nlrp3 inflammasomes represent a new regulatory mechanism of renal MBF and sodium excretion which may not depend on classical inflammatory response.
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