ArticleCell death discovery2022
TLR2/caspase-5/Panx1 pathway mediates necrosis-induced NLRP3 inflammasome activation in macrophages during acute kidney injury.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
25 citing papers in PubMed, 50 citations in OpenAlex.
- Large-Pore Channels at the Maternal-Fetal Interface: Progress and Open Research Avenues.Biology · 2026Review
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Article
- LncRNA LBX2-AS1 exacerbates LPS-induced stress on periodontal ligament cells by activating the TLR2 signaling pathway through miR-654-3p.Annals of medicine · 2025Article
- Pannexin channels in the kidney.American journal of physiology. Renal physiology · 2025Review
- Early Administration of N-Acetylcysteine Provides Renal and Cardiac Mitochondrial and Redox Protection, Preventing the Development of Cardio-Renal Syndrome Type IV Induced by 5/6NX.Antioxidants (Basel, Switzerland) · 2025Article
- Abscopal Brain Proteomic Changes Associated with Microbiome Alterations Induced by Gastrointestinal Acute Radiation Syndrome in Swine.International journal of molecular sciences · 2025Article
- Noncanonical function of Pannexin1 promotes cellular senescence and renal fibrosis post-acute kidney injury.Nature communications · 2025Article
- Effects of Mytilus edulis derived plasmalogens against atherosclerosis via lipid metabolism and MAPK signaling pathway.NPJ science of food · 2025Article
- NLRP3 inflammasome activity and pyroptosis are involved in CD206Acta biochimica et biophysica Sinica · 2025Article
- Proximal tubule pannexin 1 contributes to mitochondrial dysfunction and cell death during acute kidney injury.American journal of physiology. Renal physiology · 2025Article
- Purinoreceptor P2X7 in Extracellular ATP-Mediated Inflammation through the Spectrum of Kidney Diseases and Kidney Transplantation.Journal of the American Society of Nephrology : JASN · 2025Review
- Inflammasomes: novel therapeutic targets for metabolic syndrome?Frontiers in endocrinology · 2025Review
- Immunoregulatory programs in anti-N-methyl-D-aspartate receptor encephalitis identified by single-cell multi-omics analysis.Clinical and translational medicine · 2025Article
- The multifaceted role of macrophages in kidney physiology and diseases.Frontiers in immunology · 2025Review
- The role of the interplay between macrophage glycolytic reprogramming and NLRP3 inflammasome activation in acute lung injury/acute respiratory distress syndrome.Clinical and translational medicine · 2024Review
- Baicalin and probenecid protect against Glaesserella parasuis challenge in a piglet model.Veterinary research · 2024Article
- Renal macrophages and NLRP3 inflammasomes in kidney diseases and therapeutics.Cell death discovery · 2024Review
- Activation of Pannexin-1 channels causes cell dysfunction and damage in mesangial cells derived from angiotensin II-exposed mice.Frontiers in cell and developmental biology · 2024Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Acute kidney injury (AKI) is characterized by necroinflammation formed by necrotic tubular epithelial cells (TECs) and interstitial inflammation. In necroinflammation, macrophages are key inflammatory cells and can be activated and polarized into proinflammatory macrophages. Membranous Toll-like receptors (TLRs) can cooperate with intracellular NOD-like receptor protein 3 (NLRP3) to recognize danger signals from necrotic TECs and activate proinflammatory macrophages by assembling NLRP3 inflammasome. However, the cooperation between TLRs and NLRP3 is still unclear. Using conditioned medium from necrotic TECs, we confirmed that necrotic TECs could release danger signals to activate NLRP3 inflammasome in macrophages. We further identified that necrotic TECs-induced NLRP3 inflammasome activation was dependent on ATP secretion via Pannexin-1 (Panx1) channel in macrophages. Next, we verified that TLR2 was required for the activation of Panx1 and NLRP3 in macrophages. Mechanistically, we indicated that caspase-5 mediated TLR2-induced Panx1 activation. In addition, we showed that necrotic TECs-induced activation of TLR2/caspase-5/Panx1 axis could be decreased in macrophages when TECs was protected by N-acetylcysteine (NAC). Overall, we demonstrate that danger signals from necrotic TECs could activate NLRP3 inflammasome in macrophages via TLR2/caspase-5/Panx1 axis during AKI.
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.