ArticleKidney international2015
Phosphorylation of ribosomal protein S6 mediates compensatory renal hypertrophy.
Article in Kidney international, 2015. 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, 32 citations in OpenAlex.
- Empagliflozin, Linagliptin, and Metformin Differentially Affect Renal PI3K/Akt and MAPK/ERK Signaling Pathways inInternational journal of molecular sciences · 2026Article
- Immune cells during compensatory renal hypertrophy after unilateral nephrectomy.Research square · 2026Article
- Sodium-glucose cotransporter 2 inhibitor ameliorates podocyte hypertrophic stress by suppressing the mTOR/p70S6K/cyclin D1 signaling pathway in obesity-related nephropathy.Scientific reports · 2026Article
- Dietary methionine mitigates immune-mediated damage by enhancing renal clearance of cytokines.Cell metabolism · 2026Article
- Effect of anti-obesity drug orlistat (Xenical™) on liver and kidney function in male rats fed a high-fat diet.F1000Research · 2026Article
- Pik3c3 expression profiling in the mouse kidney and its role in proximal tubule cell physiology.American journal of physiology. Cell physiology · 2024Article
- The transcriptome of early compensatory kidney growth reveals cell and time specific responses.iScience · 2024Article
- An Ultrasensitive Room-Temperature HSensors (Basel, Switzerland) · 2024Article
- BI-D1870 Induces Mitotic Dysfunction and Apoptosis in Neuroblastoma by Regulating the PI3K-Akt-mTORC1 Signal Axis.Cancers · 2023Article
- Blocking ribosomal protein S6 phosphorylation inhibits podocyte hypertrophy and focal segmental glomerulosclerosis.Kidney international · 2022Article
- Molecular Mechanisms of Parathyroid Disorders in Chronic Kidney Disease.Metabolites · 2022Review
- Phosphorylation of ribosomal protein S6 differentially affects mRNA translation based on ORF length.Nucleic acids research · 2021Article
- CDCP1 promotes compensatory renal growth by integrating Src and Met signaling.Life science alliance · 2021Article
- Cre/loxP approach-mediated downregulation of Pik3c3 inhibits the hypertrophic growth of renal proximal tubule cells.Journal of cellular physiology · 2020Article
- Parathyroid Cell Proliferation in Secondary Hyperparathyroidism of Chronic Kidney Disease.International journal of molecular sciences · 2020Review
- The expression level of class III phosphatidylinositol-3 kinase controls the degree of compensatory nephron hypertrophy.American journal of physiology. Renal physiology · 2020Article
- Metformin effectively treatsCell death discovery · 2020Article
- Marmoset as a Model to Study Kidney Changes Associated With Aging.The journals of gerontology. Series A, Biological sciences and medical sciences · 2019Article
- Knockdown of ribosomal protein S15A inhibits human kidney cancer cell growth in vitro and in vivo.Molecular medicine reports · 2019Article
- Reducing mTOR augments parietal epithelial cell density in a model of acute podocyte depletion and in aged kidneys.American journal of physiology. Renal physiology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The molecular mechanism underlying renal hypertrophy and progressive nephron damage remains poorly understood. Here we generated congenic ribosomal protein S6 (rpS6) knock-in mice expressing nonphosphorylatable rpS6 and found that uninephrectomy-induced renal hypertrophy was significantly blunted in these knock-in mice. Uninephrectomy-induced increases in cyclin D1 and decreases in cyclin E in the remaining kidney were attenuated in the knock-in mice compared with their wild-type littermates. Uninephrectomy induced rpS6 phosphorylation in the wild-type mice; however, no rpS6 phosphorylation was detected in uninephrectomized or sham-operated knock-in mice. Nonetheless, uninephrectomy stimulated comparable 4E-BP1 phosphorylation in both knock-in and wild-type mice, indicating that mTORC1 was still activated in the knock-in mice. Moreover, the mTORC1 inhibitor rapamycin prevented both rpS6 and 4E-BP1 phosphorylation, significantly blunted uninephrectomy-induced renal hypertrophy in wild-type mice, but did not prevent residual renal hypertrophy despite inhibiting 4E-BP1 phosphorylation in uninephrectomized knock-in mice. Thus, both genetic and pharmacological approaches unequivocally demonstrate that phosphorylated rpS6 is a downstream effector of the mTORC1-S6K1 signaling pathway mediating renal hypertrophy. Hence, rpS6 phosphorylation facilitates the increase in cyclin D1 and decrease in cyclin E1 that underlie the hypertrophic nature of uninephrectomy-induced kidney growth.
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.