ArticleDiabetologia2012
Translationally controlled tumour protein is associated with podocyte hypertrophy in a mouse model of type 1 diabetes.
Article in Diabetologia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Cell cycle disorders in podocytes: an emerging and increasingly recognized phenomenon.Cell death discovery · 2025Review
- Review
- GOLPH3 protein controls organ growth by interacting with TOR signaling proteins in Drosophila.Cell death & disease · 2022Article
- Imaging the Kidney with an Unconventional Scanning Electron Microscopy Technique: Analysis of the Subpodocyte Space in Diabetic Mice.International journal of molecular sciences · 2022Article
- Article
- The role of extracellular vesicles in podocyte autophagy in kidney disease.Journal of cell communication and signaling · 2021Review
- Diabetic condition induces hypertrophy and vacuolization in glomerular parietal epithelial cells.Scientific reports · 2021Article
- Review
- Regulation of epithelial integrity and organ growth by Tctp and Coracle in Drosophila.PLoS genetics · 2020Article
- Podocyte Lysosome Dysfunction in Chronic Glomerular Diseases.International journal of molecular sciences · 2020Review
- Research Progress on the Pathological Mechanisms of Podocytes in Diabetic Nephropathy.Journal of diabetes research · 2020Review
- Long noncoding RNA ENSRNOG00000037522 is involved in the podocyte epithelial‑mesenchymal transition in diabetic rats.International journal of molecular medicine · 2018Article
- C1-Ten is a PTPase of nephrin, regulating podocyte hypertrophy through mTORC1 activation.Scientific reports · 2017Article
- Insights into the role and regulation of TCTP in skeletal muscle.Oncotarget · 2017Article
- Over-expression of insulin-response element binding protein-1 (IRE-BP1) in mouse pancreatic islets increases expression of RACK1 and TCTP: Beta cell markers of high glucose sensitivity.Biochimica et biophysica acta. Proteins and proteomics · 2017Article
- Research Progress on Mechanism of Podocyte Depletion in Diabetic Nephropathy.Journal of diabetes research · 2017Review
- The role of local IL6/JAK2/STAT3 signaling in high glucose-induced podocyte hypertrophy.Kidney research and clinical practice · 2016Article
- 14-3-3 proteins regulate Tctp-Rheb interaction for organ growth in Drosophila.Nature communications · 2016Article
- Translationally controlled tumor protein induces epithelial to mesenchymal transition and promotes cell migration, invasion and metastasis.Scientific reports · 2015Article
- Translationally controlled tumor protein is a novel biological target for neurofibromatosis type 1-associated tumors.The Journal of biological chemistry · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisTranslationally controlled tumour protein (TCTP) is thought to be involved in cell growth by regulating mTOR complex 1 (mTORC1) signalling. As diabetes characteristically induces podocyte hypertrophy and mTORC1 has been implicated in this process, TCTP may have a role in the pathogenesis of diabetes-induced podocyte hypertrophy.
methodsWe investigated the effects and molecular mechanisms of TCTP in diabetic mice and in high glucose-stimulated cultured podocytes. To characterise the role of TCTP, we conducted lentivirus-mediated gene silencing of TCTP both in vivo and in vitro.
resultsGlomerular production of TCTP was significantly higher in streptozotocin induced-diabetic DBA/2J mice than in control animals. Double-immunofluorescence staining for TCTP and synaptopodin revealed that podocyte was the principal cell responsible for this increase. TCTP knockdown attenuated the activation of mTORC1 downstream effectors and the overproduction of cyclin-dependent kinase inhibitors (CKIs) in diabetic glomeruli, along with a reduction in proteinuria and a decrease in the sizes of podocytes as well as glomeruli. In addition, knockdown of TCTP in db/db mice prevented the development of diabetic nephropathy, as indicated by the amelioration of proteinuria, mesangial expansion, podocytopenia and glomerulosclerosis. In accordance with the in vivo data, TCTP inhibition abrogated high glucose-induced hypertrophy in cultured podocytes, which was accompanied by the downregulation of mTORC1 effectors and CKIs. CONCLUSIONS/
interpretationThese findings suggest that TCTP might play an important role in the process of podocyte hypertrophy under diabetic conditions via the regulation of mTORC1 activity and the induction of cell-cycle arrest.
Indexed as
Identifiers
What OpenQuestion holds
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.