ArticleBritish journal of pharmacology2009
Inhibiting glycogen synthase kinase-3 reduces endotoxaemic acute renal failure by down-regulating inflammation and renal cell apoptosis.
Article in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- Molecular mechanisms in lithium-associated renal disease: a systematic review.International urology and nephrology · 2016Pooled it
- Research Progress of Antioxidants in Oxidative Stress Therapy after Spinal Cord Injury.Neurochemical research · 2023Review
- Dietary lithium intake, graft failure and mortality in kidney transplant recipients.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023Article
- Lithium in Cancer Therapy: Friend or Foe?Cancers · 2023Review
- Lithium promotes recovery after spinal cord injury.Neural regeneration research · 2022Article
- Role of Glycogen Synthase Kinase-3 in Interferon-γ-Mediated Immune Hepatitis.International journal of molecular sciences · 2022Review
- Age-related GSK3β overexpression drives podocyte senescence and glomerular aging.The Journal of clinical investigation · 2022Article
- Article
- Pharmacologically Inhibiting Glycogen Synthase Kinase-3β Ameliorates Renal Inflammation and Nephrotoxicity in an Animal Model of Cisplatin-Induced Acute Kidney Injury.Biomedicines · 2021Article
- Lithium Chloride Protects against Sepsis-Induced Skeletal Muscle Atrophy and Cancer Cachexia.Cells · 2021Article
- GSK3 inhibitor-loaded osteotropic Pluronic hydrogel effectively mitigates periodontal tissue damage associated with experimental periodontitis.Biomaterials · 2020Article
- Glycogen synthase kinase-3β inhibits tubular regeneration in acute kidney injury by a FoxM1-dependent mechanism.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Article
- Review
- GSK3β-mediated Keap1-independent regulation of Nrf2 antioxidant response: A molecular rheostat of acute kidney injury to chronic kidney disease transition.Redox biology · 2019Article
- Thinking forward: promising but unproven ideas for future intensive care.Critical care (London, England) · 2019Article
- Lithium ameliorates tubule-interstitial injury through activation of the mTORC2/protein kinase B pathway.PloS one · 2019Article
- Aged kidney: can we protect it? Autophagy, mitochondria and mechanisms of ischemic preconditioning.Cell cycle (Georgetown, Tex.) · 2018Article
- Animal models for bipolar disorder: from bedside to the cage.International journal of bipolar disorders · 2017Review
- Effects of chronic alcohol exposure on ischemia-reperfusion-induced acute kidney injury in mice: the role of β-arrestin 2 and glycogen synthase kinase 3.Experimental & molecular medicine · 2017Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeExcessive inflammation and apoptosis are pathological features of endotoxaemic acute renal failure. Activation of glycogen synthase kinase-3 (GSK-3) is involved in inflammation and apoptosis. We investigated the effects of inhibiting GSK-3 on lipopolysaccharide (LPS)-induced acute renal failure, nuclear factor-kappaB (NF-kappaB), inflammation and apoptosis. EXPERIMENTAL APPROACH: The effects of inhibiting GSK-3 with inhibitors, including lithium chloride (LiCl) and 6-bromo-indirubin-3'-oxime (BIO), on LPS-treated (15 mg x kg(-1)) C3H/HeN mice (LiCl, 40 mg x kg(-1) and BIO, 2 mg x kg(-1)) and LPS-treated (1 microg x mL(-1)) renal epithelial cells (LiCl, 20 mM and BIO, 5 microM) were studied. Mouse survival was monitored and renal function was analysed by histological and serological examination. Cytokine and chemokine production, and cell apoptosis were measured by enzyme-linked immunosorbent assay and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labelling staining, respectively. Activation of NF-kappaB and GSK-3 was determined by immunostaining and Western blotting, respectively. KEY
resultsMice treated with GSK-3 inhibitors showed decreased mortality, renal tubular dilatation, vacuolization and sloughing, blood urea nitrogen, creatinine and renal cell apoptosis in response to endotoxaemia. Inhibiting GSK-3 reduced LPS-induced tumour necrosis factor-alpha (TNF-alpha) and CCL5/RANTES (released upon activation of normal T-cells) in vivo in mice and in vitro in murine kidney cortical collecting duct epithelial M1 cells. Inhibiting GSK-3 did not block TNF-alpha-induced cytotoxicity in rat kidney proximal tubular epithelial NRK52E or in M1 cells. CONCLUSIONS AND IMPLICATIONS: These results suggest that GSK-3 inhibition protects against endotoxaemic acute renal failure mainly by down-regulating pro-inflammatory TNF-alpha and RANTES.
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