ArticleThe American journal of pathology1998
Polycystic kidney disease in SBM transgenic mice: role of c-myc in disease induction and progression.
Article in The American journal of pathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 81 citations in OpenAlex.
- Kcnn4/KCa3.1 inhibition blunts polycystic kidney disease progression in mouse models.JCI insight · 2025Article
- Differential regulation of MYC expression byFrontiers in cell and developmental biology · 2023Article
- Enhancer and super-enhancer landscape in polycystic kidney disease.Kidney international · 2023Article
- Cystin genetic variants cause autosomal recessive polycystic kidney disease associated with altered Myc expression.Scientific reports · 2021Article
- A methionine-Mettl3-NCell metabolism · 2021Article
- An Overview of In Vivo and In Vitro Models for Autosomal Dominant Polycystic Kidney Disease: A Journey from 3D-Cysts to Mini-Pigs.International journal of molecular sciences · 2020Review
- Apoptosis and autophagy in polycystic kidney disease (PKD).Cellular signalling · 2020Review
- c-Myc is a regulator of the PKD1 gene and PC1-induced pathogenesis.Human molecular genetics · 2019Article
- Casein kinase 1ε and 1α as novel players in polycystic kidney disease and mechanistic targets for (R)-roscovitine and (S)-CR8.American journal of physiology. Renal physiology · 2018Article
- microRNA-17 family promotes polycystic kidney disease progression through modulation of mitochondrial metabolism.Nature communications · 2017Article
- Autosomal Dominant Polycystic Disease is Associated with Depressed Levels of Soluble Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand.Balkan medical journal · 2016Article
- Ouabain Enhances ADPKD Cell Apoptosis via the Intrinsic Pathway.Frontiers in physiology · 2016Article
- An mTOR kinase inhibitor slows disease progression in a rat model of polycystic kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2015Article
- Generation of c-Myc transgenic pigs for autosomal dominant polycystic kidney disease.Transgenic research · 2013Article
- Polycystins and cellular Ca2+ signaling.Cellular and molecular life sciences : CMLS · 2013Review
- The ciliary protein cystin forms a regulatory complex with necdin to modulate Myc expression.PloS one · 2013Article
- mTORC1/2 and rapamycin in female Han:SPRD rats with polycystic kidney disease.American journal of physiology. Renal physiology · 2011Article
- Transgenic overexpression of Anks6(p.R823W) causes polycystic kidney disease in rats.The American journal of pathology · 2010Article
- Mutant polycystin-2 induces proliferation in primary rat tubular epithelial cells in a STAT-1/p21-independent fashion accompanied instead by alterations in expression of p57KIP2 and Cdk2.BMC nephrology · 2008Article
- Caspase-3 gene deletion prolongs survival in polycystic kidney disease.Journal of the American Society of Nephrology : JASN · 2008Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
SBM mouse is a unique transgenic model of polycystic kidney disease (PKD) produced by dysregulation of c-myc in the kidneys. Our previous demonstration that c-myc is overexpressed in human autosomal polycystic kidney disease (ADPKD) prompted us to investigate the pathogenetic role of c-myc in the induction and progression of the cystogenic phenotype in our mouse model. In young SBM kidneys, c-myc was two- to threefold increased with persistent expression levels into adulthood, an age when c-myc is normally undetectable. In situ hybridization analysis of the c-myc transgene demonstrated intense signal specifically overlying glomerular and tubular epithelium of developing cysts in fetal and young kidneys. Increased expression of c-myc correlated with the initiation and progression of the PKD phenotype as evidenced by early tubular and glomerular cysts at E16.5. Cyst number and size increased with age, with co-development of glomerular and tubular epithelial hyperplasia. Consistently, the mean renal proliferative index was increased approximately 5- to 20-fold in noncystic and cystic tubules of newborn SBM animals compared with littermate controls. Similarly, in fetal and newborn kidneys the tubular apoptotic indices were increased approximately three- to ninefold over controls. Both proliferation and apoptotic rates in cystic tubules approached levels in developing tubules from the normal nephrogenic zone. We conclude that the pathogenesis of PKD hinges on a critical imbalance in c-myc regulation of the opposing processes of cell proliferation and apoptosis, recapitulating the cellular phenomena in developing fetal kidney.
Indexed as
Identifiers
9422539PMC1858107W48044147What 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.