ArticleDiabetes2012
Hyperglycemia causes renal cell damage via CCN2-induced activation of the TrkA receptor: implications for diabetic nephropathy.
Article in Diabetes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 26 citations in OpenAlex.
- Unveiling the TrkA-p35/CDK5 axis: a novel therapeutic target in diabetic kidney disease.Frontiers in endocrinology · 2026Article
- Yifei Decoction Regulates the NGF/TRKA/PI3K/AKT Signaling Axis to Inhibit the Epithelial-Mesenchymal Transformation and Proliferation of Pulmonary Epithelial Cells in Bleomycin-Induced Pulmonary Fibrogenesis.Canadian respiratory journal · 2026Article
- Ntrk1 promotes mesangial cell proliferation and inflammation in rat glomerulonephritis model by activating the STAT3 and p38/ERK MAPK signaling pathways.BMC nephrology · 2022Article
- Conjunction junction, what's the function? CCN proteins as targets in fibrosis and cancers.American journal of physiology. Cell physiology · 2020Review
- Renal expression of JAK2 is high in polycystic kidney disease and its inhibition reduces cystogenesis.Scientific reports · 2019Article
- Targeting Phospholipase D4 Attenuates Kidney Fibrosis.Journal of the American Society of Nephrology : JASN · 2017Article
- Synthesis of substituted 2MedChemComm · 2017Article
- Yin and Yang revisited: CCN3 as an anti-fibrotic therapeutic?Journal of cell communication and signaling · 2015Article
- The interplay between glucose and fatty acids on tube formation and fatty acid uptake in the first trimester trophoblast cells, HTR8/SVneo.Molecular and cellular biochemistry · 2015Article
- Fell-Muir lecture: Connective tissue growth factor (CCN2) -- a pernicious and pleiotropic player in the development of kidney fibrosis.International journal of experimental pathology · 2013Article
- Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
CCN2, a secreted profibrotic protein, is highly expressed in diabetic nephropathy (DN) and implicated in its pathogenesis; however, the actions of CCN2 in DN remain elusive. We previously demonstrated that CCN2 triggers signaling via tropomyosin receptor kinase A (TrkA). Trace expression of TrkA is found in normal kidneys, but its expression is elevated in several nephropathies; yet its role in DN is unexplored. In this study we show de novo expression of TrkA in human and murine DN. We go on to study the molecular mechanisms leading to TrkA activation and show that it involves hypoxia, as demonstrated by ischemia-reperfusion injury and in vitro experiments mimicking hypoxia, implicating hypoxia as a common pathway leading to disease. We also expose renal cells to hyperglycemia, which led to TrkA phosphorylation in mesangial cells, tubular epithelial cells, and podocytes but not in glomerular endothelial cells and renal fibroblasts. In addition, we report that hyperglycemia caused an induction of phosphorylated extracellular signal-related kinase 1/2 and Snail1 that was abrogated by silencing of TrkA or CCN2 using small interfering RNA. In conclusion, we provide novel evidence that TrkA is activated in diabetic kidneys and suggest that anti-TrkA therapy may prove beneficial in DN.
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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.