ReviewCell death discovery2024
Renal macrophages and NLRP3 inflammasomes in kidney diseases and therapeutics.
Review in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
54 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Nanomaterial-Based Precision Drug Delivery for Advanced Nephrology Therapy: A Systematic Review.International journal of nanomedicine · 2026Pooled it
- Targeting Interleukin-6 for Treatment of CKD and Cardiovascular Disease.Kidney international reports · 2026Review
- Disulfiram Attenuates Adenine-Induced Renal Fibrosis by Modulating Inflammatory and Immunometabolic Responses.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- From xanthine oxidase inhibition to inflammasome regulation: exploring the potential role of allopurinol in TXNIP-NLRP3 signaling and pyroptosis in diabetes.Inflammopharmacology · 2026Review
- Broccoli Sprout Extract Restores Renal Lipid Metabolism in High-Fat Diet-Fed Mice Involving Modulation of AMPK/Nrf2 Signaling and the NLRP3 Inflammasome.Food science & nutrition · 2026Article
- Article
- Mechanisms of Obesity-Related Kidney Disease: From Adipose Depot Biology to the Chymase-Aldosterone and Ghrelin-Leptin Axes.Biomolecules · 2026Review
- Mechanisms by which macrophage Ltb4r1 mediates tubular epithelial cell injury to facilitate the advancement of diabetic kidney disease.BMC nephrology · 2026Article
- Macrophage-specific circular RNA circHIPK2, inflammation, and fibrosis after myocardial infarction.European heart journal · 2026Article
- Mitochondrial Regulation of the NLRP3 Inflammasome in Diabetic Kidney Disease: From Mechanisms to Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Review
- Targeting pyroptosis in renal fibrosis: From molecular mechanisms to therapeutic horizons (Review).International journal of molecular medicine · 2026Review
- Uromodulin p.His36Tyr promotes macrophage pyroptosis via App-Cd74 signaling to drive renal inflammation in ADTKD.Nature communications · 2026Article
- GAS5 mediates notch signaling to exacerbate calcium oxalate-induced renal injury through the NF-κB/NLRP3 axis by promoting macrophage polarization.Cellular and molecular life sciences : CMLS · 2026Article
- Inhibiting the P2X7R-NLRP3 inflammasome pathway regulates CXCL16 to alleviate podocyte injury in mice with adriamycin nephropathy.Scientific reports · 2026Article
- Berberine inhibits ISG15 and pyroptosis to attenuate diabetic kidney disease inflammation and fibrosis.Apoptosis : an international journal on programmed cell death · 2026Article
- A Melittin-Derived Lead Compound Ameliorates Severe Acute Pancreatitis by Restoring Oxidative Homeostasis and Macrophage Metabolism.Inflammation · 2026Article
- Inflammation and Diabetic Kidney Disease.International journal of molecular sciences · 2026Review
- A pH-Responsive Biomimetic Antioxidant Nanoplatform with Dual Renal Targeting for Synergistic Therapy of Acute Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Uric acid-associated mechanisms of coronary artery calcification in diabetic kidney disease: evidence, hypotheses, and translational perspectives.Frontiers in cardiovascular medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Macrophages are exceptionally diversified cell types and perform unique features and functions when exposed to different stimuli within the specific microenvironment of various kidney diseases. In instances of kidney tissue necrosis or infection, specific patterns associated with damage or pathogens prompt the development of pro-inflammatory macrophages (M1). These M1 macrophages contribute to exacerbating tissue damage, inflammation, and eventual fibrosis. Conversely, anti-inflammatory macrophages (M2) arise in the same circumstances, contributing to kidney repair and regeneration processes. Impaired tissue repair causes fibrosis, and hence macrophages play a protective and pathogenic role. In response to harmful stimuli within the body, inflammasomes, complex assemblies of multiple proteins, assume a pivotal function in innate immunity. The initiation of inflammasomes triggers the activation of caspase 1, which in turn facilitates the maturation of cytokines, inflammation, and cell death. Macrophages in the kidneys possess the complete elements of the NLRP3 inflammasome, including NLRP3, ASC, and pro-caspase-1. When the NLRP3 inflammasomes are activated, it triggers the activation of caspase-1, resulting in the release of mature proinflammatory cytokines (IL)-1β and IL-18 and cleavage of Gasdermin D (GSDMD). This activation process therefore then induces pyroptosis, leading to renal inflammation, cell death, and renal dysfunction. The NLRP3-ASC-caspase-1-IL-1β-IL-18 pathway has been identified as a factor in the development of the pathophysiology of numerous kidney diseases. In this review, we explore current progress in understanding macrophage behavior concerning inflammation, injury, and fibrosis in kidneys. Emphasizing the pivotal role of activated macrophages in both the advancement and recovery phases of renal diseases, the article delves into potential strategies to modify macrophage functionality and it also discusses emerging approaches to selectively target NLRP3 inflammasomes and their signaling components within the kidney, aiming to facilitate the healing process in kidney diseases.
Identifiers
What OpenQuestion holds
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.