ArticleCirculation research2022
Tubular IL-1β Induces Salt Sensitivity in Diabetes by Activating Renal Macrophages.
Article in Circulation research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 47 citations in OpenAlex.
- Molecular and Cellular Underpinnings of Primary Hypertension: An Integrative Mechanistic Framework.Journal of cellular physiology · 2026Review
- Nanomedicine beyond carriers - devices, cells & living therapeutics.Biomedical microdevices · 2026Review
- Polymeric mesoscale nanoparticles exhibit dynamin- and macropinocytosis-dependent endocytosis.Nanomedicine : nanotechnology, biology, and medicine · 2026Article
- Salt and chronic kidney disease.Nature reviews. Nephrology · 2026Review
- High-salt diet in macrophage-associated metabolic disorders: Mechanisms and therapeutic implications.Chinese medical journal · 2026Review
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- LncRNA Gm16023 limits M1 macrophage-mediated hyperglycemia-exacerbated septic intestinal injury via miR-377-3p/Sirt1 axis.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- The HDAC1 inhibitor attenuates renal ischemia-reperfusion injury via dual epigenetic modulation of p53 and macrophage NF-κB pathways.Cell biology and toxicology · 2026Article
- A programmable nanoreactor for photothermal immunotherapy via NIR-II triggered enzyme-catalyzed immunogenic tumor microenvironment remodeling.Asian journal of pharmaceutical sciences · 2026Article
- Decreased potential for lymphatic vessel generation is a hallmark of early diagnosed arterial hypertension and can be reversed by treatment with angiotensin converting enzyme inhibitors.Scientific reports · 2026Article
- The expanding role of Nogo-B in hypertension: linking kidney physiology, endothelial function and inflammation.Journal of hypertension · 2026Review
- Matricellular protein SMOC2 safeguards tubular integrity in acute kidney injury via integrin β3-dependent inhibition of CCND1-CDK4/6 axis.Molecular biomedicine · 2026Article
- Endocytosis of PEGylated polymeric mesoscale nanoparticles is dynamin- and macropinocytosis-dependent.bioRxiv : the preprint server for biology · 2026Article
- Inflammation and Diabetic Kidney Disease.International journal of molecular sciences · 2026Review
- Innovative Insights into Interleukin-Mediated Macrophage Polarization: Metabolic Reprogramming and Inflammatory Pathway Crosstalk in Chronic Kidney Disease and Therapeutic Implications-A Narrative Review.International journal of general medicine · 2026Review
- Translational Nanomedicine and Delivery Tools for Cardiovascular Disease Therapy and Diagnostics.Advances in experimental medicine and biology · 2026Review
- Pathways to translation for nanomedicine in nephrology.Clinical kidney journal · 2025Review
- Article
- Observation of the Effects of Different Enzyme Digestion Time and Enzyme Digestion Methods on the Extraction of Primary Renal Tubular Epithelial Cells from Sprague-Dawley Suckling Mice.Biochemical genetics · 2025Article
- Crosstalk between ferroptosis and innate immune in diabetic kidney disease: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundChronic renal inflammation has been widely recognized as a major promoter of several forms of high blood pressure including salt-sensitive hypertension. In diabetes, IL (interleukin)-6 induces salt sensitivity through a dysregulation of the epithelial sodium channel. However, the origin of this inflammatory process and the molecular events that culminates with an abnormal regulation of epithelial sodium channel and salt sensitivity in diabetes are largely unknown.
methodsBoth in vitro and in vivo approaches were used to investigate the molecular and cellular contributors to the renal inflammation associated with diabetic kidney disease and how these inflammatory components interact to develop salt sensitivity in db/db mice.
resultsThirty-four-week-old db/db mice display significantly higher levels of IL-1β in renal tubules compared with nondiabetic db/+ mice. Specific suppression of IL-1β in renal tubules prevented salt sensitivity in db/db mice. A primary culture of renal tubular epithelial cells from wild-type mice releases significant levels of IL-1β when exposed to a high glucose environment. Coculture of tubular epithelial cells and bone marrow-derived macrophages revealed that tubular epithelial cell-derived IL-1β promotes the polarization of macrophages towards a proinflammatory phenotype resulting in IL-6 secretion. To evaluate whether macrophages are the cellular target of IL-1β in vivo, diabetic db/db mice were transplanted with the bone marrow of IL-1R1 (IL-1 receptor type 1) knockout mice. db/db mice harboring an IL-1 receptor type 1 knockout bone marrow remained salt resistant, display lower renal inflammation and lower expression and activity of epithelial sodium channel compared with db/db transplanted with a wild-type bone marrow.
conclusionsRenal tubular epithelial cell-derived IL-1β polarizes renal macrophages towards a proinflammatory phenotype that promotes salt sensitivity through the accumulation of renal IL-6. When tubular IL-1β synthesis is suppressed or in db/db mice in which immune cells lack the IL-1R1, macrophage polarization is blunted resulting in no salt-sensitive hypertension.
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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.