ArticlePloS one2014
The early activation of toll-like receptor (TLR)-3 initiates kidney injury after ischemia and reperfusion.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Loss of C3 and CD14 reduces region-specific neuroinflammation in a murine polytrauma model.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- A novel two-hit murine model of viral-primed sepsis-associated acute kidney injury.American journal of physiology. Renal physiology · 2026Article
- Cytosolic nucleic acid sensing as driver of critical illness: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2025Review
- Neutrophil extracellular trap-derived double-stranded RNA aggravates PANoptosis in renal ischemia reperfusion injury.Cell communication and signaling : CCS · 2025Article
- Protective effects of pioglitazone in renal ischemia-reperfusion injury (RIRI): focus on oxidative stress and inflammation.Clinical and experimental nephrology · 2024Review
- Human pulmonary microvascular endothelial cells respond to DAMPs from injured renal tubular cells.Pulmonary circulation · 2024Article
- Lipotoxicity and immunometabolism in ischemic acute kidney injury: current perspectives and future directions.Frontiers in pharmacology · 2024Review
- Prunetin in a GPR30-dependent manner mitigates renal ischemia/reperfusion injury in rats via interrupting indoxyl sulfate/TLR4/TRIF, RIPK1/RIPK3/MLKL, and RIPK3/PGAM5/DRP-1 crosstalk.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023Article
- Simultaneous C5 and CD14 inhibition limits inflammation and organ dysfunction in pig polytrauma.Frontiers in immunology · 2022Article
- Aminoguanidine Prevents the Oxidative Stress, Inhibiting Elements of Inflammation, Endothelial Activation, Mesenchymal Markers, and Confers a Renoprotective Effect in Renal Ischemia and Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2021Article
- Review
- A Cell-Penetrating Peptide That Blocks Toll-Like Receptor Signaling Protects Kidneys against Ischemia-Reperfusion Injury.International journal of molecular sciences · 2021Article
- Toll-Like Receptors in Acute Kidney Injury.International journal of molecular sciences · 2021Review
- Overexpression of TOLLIP Protects against Acute Kidney Injury after Paraquat Intoxication through Inhibiting NLRP3 Inflammasome Activation Modulated by Toll-Like Receptor 2/4 Signaling.Mediators of inflammation · 2021Article
- Toll-Like Receptor as a Potential Biomarker in Renal Diseases.International journal of molecular sciences · 2020Review
- Metabolic Flexibility and Innate Immunity in Renal Ischemia Reperfusion Injury: The Fine Balance Between Adaptive Repair and Tissue Degeneration.Frontiers in immunology · 2020Review
- Initiation of the inflammatory response after renal ischemia/reperfusion injury during renal transplantation.International urology and nephrology · 2018Review
- Risk of long-term anticoagulation under sustained severe arterial hypertension: A translational study comparing warfarin and the new oral anticoagulant apixaban.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- Expression of TLR2, NOD1, and NOD2 and the NLRP3 Inflammasome in Renal Tubular Epithelial Cells of Male versus Female Mice.Nephron · 2017Article
- [The 22nd annual meeting of the working group for kidney transplantation of the German Society of Urology in Rostock].Der Urologe. Ausg. A · 2015Article
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) is one of the most important complications in hospitalized patients and its pathomechanisms are not completely elucidated. We hypothesize that signaling via toll-like receptor (TLR)-3, a receptor that is activated upon binding of double-stranded nucleotides, might play a crucial role in the pathogenesis of AKI following ischemia and reperfusion (IR). Male adult C57Bl6 wild-type (wt) mice and TLR-3 knock-out (-/-) mice were subjected to 30 minutes bilateral selective clamping of the renal artery followed by reperfusion for 30 min 2.5h and 23.5 hours or subjected to sham procedures. TLR-3 down-stream signaling was activated already within 3 h of ischemia and reperfusion in post-ischemic kidneys of wt mice lead to impaired blood perfusion followed by a strong pro-inflammatory response with significant neutrophil invasion. In contrast, this effect was absent in TLR-3-/- mice. Moreover, the quick TLR-3 activation resulted in kidney damage that was histomorphologically associated with significantly increased apoptosis and necrosis rates in renal tubules of wt mice. This finding was confirmed by increased kidney injury marker NGAL in wt mice and a better preserved renal perfusion after IR in TLR-3-/- mice than wt mice. Overall, the absence of TLR-3 is associated with lower cumulative kidney damage and maintained renal blood perfusion within the first 24 hours of reperfusion. Thus, we conclude that TLR-3 seems to participate in the pathogenesis of early acute kidney injury.
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