ReviewActa physiologica (Oxford, England)2017
Physiological aspects of Toll-like receptor 4 activation in sepsis-induced acute kidney injury.
Review in Acta physiologica (Oxford, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 69 citations in OpenAlex.
- Early immune anergy towards recall antigens and mitogens in patients at onset of septic shock.Scientific reports · 2018Trial
- Gut microbiota and sepsis-associated acute kidney injury: a narrative review.Frontiers in immunology · 2026Review
- Xuebijing injection alleviates septic acute kidney injury by modulating inflammation, mitochondrial dysfunction, and endoplasmic reticulum stress.Renal failure · 2025Article
- Cilastatin Attenuates Acute Kidney Injury and Reduces Mortality in a Rat Model of Sepsis.International journal of molecular sciences · 2025Article
- Role of Central Inflammatory and Oxidative Pathways in the Morphine Exacerbation of Cardiovascular Effects of Sepsis in Rats.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Multiple Signaling Axes (TNF-α/IL1β/IL8, TLR4/MYD88/NF-κB, and TGF-β1/ROS) Associated With Coronary Collateral Circulation of Coronary Chronic Total Occlusion in Geriatric Patients.Mediators of inflammation · 2025Article
- Inflammatory and chemotactic signals of the brainstem solitary tract mediate the morphine exacerbation of impaired reflex chronotropism in septic rats.Frontiers in pharmacology · 2025Article
- Renal tubular epithelial cells response to injury in acute kidney injury.EBioMedicine · 2024Review
- Protective Role of MAVS Signaling for Murine Lipopolysaccharide-Induced Acute Kidney Injury.ImmunoHorizons · 2024Article
- Decoding nature: multi-target anti-inflammatory mechanisms of natural products in the TLR4/NF-κB pathway.Frontiers in pharmacology · 2024Review
- The Protecting Role of Black Seed Oil and Its Nano-Formulation in LPS-Induced Acute Kidney Injury in Mice: Evaluation of Oxidative Stress, Biochemical & Molecular Parameters.Journal of inflammation research · 2024Article
- Toll-like receptor 4 promotes the inflammatory response in septic acute kidney injury by promoting p38 mitogen-activated protein kinase phosphorylation.Journal of bioenergetics and biomembranes · 2023Article
- Nanodrugs alleviate acute kidney injury: Manipulate RONS at kidney.Bioactive materials · 2023Review
- Antioxidant, Antiapoptotic, and Anti-Inflammatory Effects of Hesperetin in a Mouse Model of Lipopolysaccharide-Induced Acute Kidney Injury.Molecules (Basel, Switzerland) · 2023Article
- Toll-like Receptor 4 in Acute Kidney Injury.International journal of molecular sciences · 2023Review
- Platelet-derived extracellular vesicles aggravate septic acute kidney injury via delivering ARF6.International journal of biological sciences · 2023Article
- Tryptophol Acetate and Tyrosol Acetate, Small-Molecule Metabolites Identified in a Probiotic Mixture, Inhibit Hyperinflammation.Journal of innate immunity · 2023Article
- Role of Toll-like receptor 4 in intravascular hemolysis-mediated injury.The Journal of pathology · 2022Article
- Fatty acid-binding protein 4 is a therapeutic target for septic acute kidney injury by regulating inflammatory response and cell apoptosis.Cell death & disease · 2022Article
- The Rationale and Current Status of Endotoxin Adsorption in the Treatment of Septic Shock.Journal of clinical medicine · 2022Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis-induced acute kidney injury (SI-AKI) is common and associated with high mortality. Survivors are at increased risk of chronic kidney disease. The precise mechanism underlying SI-AKI is unknown, and no curative treatment exists. Toll-like receptor 4 (TLR4) activates the innate immune system in response to exogenous microbial products. The result is an inflammatory reaction aimed at clearing a potential infection. However, the consequence may also be organ dysfunction as the immune response can cause collateral damage to host tissue. The purpose of this review is to describe the basis for how ligand binding to TLR4 has the potential to cause renal dysfunction and the mechanisms by which this may take place in gram-negative sepsis. In addition, we highlight areas for future research that can further our knowledge of the pathogenesis of SI-AKI in relation to TLR4 activation. TLR4 is expressed in the kidney. Activation of TLR4 causes cytokine and chemokine release as well as renal leucocyte infiltration. It also results in endothelial and tubular dysfunction in addition to altered renal metabolism and circulation. From a physiological standpoint, inhibiting TLR4 in large animal experimental SI-AKI significantly improves renal function. Thus, current evidence indicates that TLR4 has the ability to mediate SI-AKI by a number of mechanisms. The strong experimental evidence supporting a role of TLR4 in the pathogenesis of SI-AKI in combination with the availability of pharmacological tools to target TLR4 warrants future human studies.
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