ArticlePloS one2014
TRAIL deficiency contributes to diabetic nephropathy in fat-fed ApoE-/- mice.
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 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Monocytes as a convergent nanoparticle therapeutic target for cardiovascular diseases.Advanced drug delivery reviews · 2022Pooled it
- Article
- The generation of stable microvessels in ischemia is mediated by endothelial cell derived TRAIL.Science advances · 2024Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- The Prognostic, Diagnostic, and Therapeutic Potential of TRAIL Signalling in Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- Repositioning the Role of Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) on the TRAIL to the Development of Diabetes Mellitus: An Update of Experimental and Clinical Evidence.International journal of molecular sciences · 2022Review
- Hyperlipidemia Influences the Accuracy of Glucometer-Measured Blood Glucose Concentrations in Genetically Diverse Mice.The American journal of the medical sciences · 2021Article
- A "Western Diet" promotes symptoms of hepatic steatosis in spontaneously hypertensive rats.International journal of experimental pathology · 2020Article
- Beyond adiponectin and leptin: adipose tissue-derived mediators of inter-organ communication.Journal of lipid research · 2019Review
- TRAIL, OPG, and TWEAK in kidney disease: biomarkers or therapeutic targets?Clinical science (London, England : 1979) · 2019Review
- TRAIL-Expressing Monocyte/Macrophages Are Critical for Reducing Inflammation and Atherosclerosis.iScience · 2019Article
- Relationship between low levels of circulating TRAIL and atheromatosis progression in patients with chronic kidney disease.PloS one · 2018Article
- Non-alcoholic fatty liver disease, vascular inflammation and insulin resistance are exacerbated by TRAIL deletion in mice.Scientific reports · 2017Article
- Therapeutic applications of TRAIL receptor agonists in cancer and beyond.Pharmacology & therapeutics · 2015Review
- Elevation of circulating TNF receptors 1 and 2 increases the risk of end-stage renal disease in American Indians with type 2 diabetes.Kidney international · 2015Article
- Ventral prostate fibrosis in the Akita mouse is associated with macrophage and fibrocyte infiltration.Journal of diabetes research · 2014Article
- Tumour necrosis factor-related apoptosis-inducing ligand expression in patients with diabetic nephropathy.Journal of the renin-angiotensin-aldosterone system : JRAASArticle
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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
backgroundWe recently demonstrated that TNF-related apoptosis-inducing ligand (TRAIL) is protective of diet-induced diabetes in mice. While TRAIL has been implicated in chronic kidney disease, its role in vivo in diabetic nephropathy is not clear. The present study investigated the role of TRAIL in the pathogenesis of diabetic nephropathy using TRAIL(-/-)ApoE(-/-) mice.
methodsTRAIL(-/-)ApoE(-/-) and ApoE(-/-) mice were fed a high fat diet for 20 w. Plasma glucose and insulin levels were assessed over 0, 5, 8 and 20 w. At 20 w, markers of kidney function including creatinine, phosphate, calcium and cystatin C were measured. Changes in mRNA expression of MMPs, TIMP-1, IL-1β and IL-18 were assessed in the kidney. Functional and histological changes in kidneys were examined. Glucose and insulin tolerance tests were performed.
resultsTRAIL(-/-)ApoE(-/-) mice had significantly increased urine protein, urine protein:creatinine ratio, plasma phosphorous, and plasma cystatin C, with accelerated nephropathy. Histologically, increased extracellular matrix, mesangial expansion and mesangial cell proliferation in the glomeruli were observed. Moreover, TRAIL(-/-)ApoE(-/-) kidneys displayed loss of the brush border and disorganisation of tubular epithelium, with increased fibrosis. TRAIL-deficient kidneys also had increased expression of MMPs, TIMP-1, PAI-1, IL-1β and IL-18, markers of renal injury and inflammation. Compared with ApoE(-/-) mice, TRAIL-/-ApoE-/- mice displayed insulin resistance and type-2 diabetic features with reduced renal insulin-receptor expression.
conclusionsHere, we show that TRAIL-deficiency in ApoE(-/-) mice exacerbates nephropathy and insulin resistance. Understanding TRAIL signalling in kidney disease and diabetes, may therefore lead to novel strategies for the treatment of diabetic nephropathy.
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