ArticleCell metabolism2016
Interleukin-1 Receptor Activation Potentiates Salt Reabsorption in Angiotensin II-Induced Hypertension via the NKCC2 Co-transporter in the Nephron.
Article in Cell metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
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Who cites it
93 citing papers in PubMed, 146 citations in OpenAlex.
- Effects of Interleukin-1β Inhibition on Blood Pressure, Incident Hypertension, and Residual Inflammatory Risk: A Secondary Analysis of CANTOS.Hypertension (Dallas, Tex. : 1979) · 2020Trial
- Molecular and Cellular Underpinnings of Primary Hypertension: An Integrative Mechanistic Framework.Journal of cellular physiology · 2026Review
- Review
- Inflammation and oxidative stress are associated with major adverse cardiovascular events in adults with preclinical hypertension.Scientific reports · 2025Observational
- Paradoxical sex differences in a hamster model of angiotensin II-dependent hypertension and associated renal injury.Biology of sex differences · 2025Article
- Uric Acid and Preeclampsia: Pathophysiological Interactions and the Emerging Role of Inflammasome Activation.Antioxidants (Basel, Switzerland) · 2025Review
- A new era in the treatment of kidney diseases: NLRP3 inflammasome and cytokine-targeted therapies.Pediatric nephrology (Berlin, Germany) · 2025Review
- Epithelial Na+ Channels, Immune Cells, and Salt.Annual review of physiology · 2025Review
- VEGFR3 mitigates hypertensive nephropathy by enhancing mitophagy via regulating crotonylation of HSPA1L.Cell communication and signaling : CCS · 2025Article
- Epigenetic Regulation of Innate and Adaptive Immune Cells in Salt-Sensitive Hypertension.Circulation research · 2025Review
- Targeting interleukin-1 signaling for renoprotection.Frontiers in immunology · 2025Review
- The immune-microbiome axis in salt-sensitive hypertension: a focus on renal and neural mechanisms.Frontiers in physiology · 2025Review
- Understanding COVID-19-related Acute Renal Injury in Elderly Individuals: Preexisting Systemic Inflammation before COVID-19 (SIC).Endocrine, metabolic & immune disorders drug targets · 2025Article
- CaInflammation and regeneration · 2024Review
- Article
- Experimental TET2 Clonal Hematopoiesis Predisposes to Renal Hypertension Through an Inflammasome-Mediated Mechanism.Circulation research · 2024Article
- IL-1R Mediated Activation of Renal Sensory Nerves in DOCA-Salt Hypertension.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Immune Mechanisms in Hypertension.Hypertension (Dallas, Tex. : 1979) · 2024Review
- The Multifaceted Nature of Macrophages in Cardiovascular Disease.Biomedicines · 2024Review
- Immune and inflammatory mechanisms in hypertension.Nature reviews. Cardiology · 2024Review
33 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Hypertension is among the most prevalent and catastrophic chronic diseases worldwide. While the efficacy of renin angiotensin system (RAS) blockade in lowering blood pressure illustrates that the RAS is broadly activated in human hypertension, the frequent failure of RAS inhibition to prevent or reverse hypertensive organ damage highlights the need for novel therapies to combat RAS-dependent hypertension. We previously discovered elevated levels of the macrophage cytokine IL-1 in the kidney in a murine model of RAS-mediated hypertension. Here we report that IL-1 receptor (IL-1R1) deficiency or blockade limits blood pressure elevation in this model by mitigating sodium reabsorption via the NKCC2 co-transporter in the nephron. In this setting, IL-1R1 activation prevents intra-renal myeloid cells from maturing into Ly6C(+)Ly6G(-) macrophages that elaborate nitric oxide, a natriuretic hormone that suppresses NKCC2 activity. By revealing how the innate immune system regulates tubular sodium transport, these experiments should lead to new immunomodulatory anti-hypertensive therapies.
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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 OpenQuestion graph.