Evidence map›Paper›PMID 25904703›Full record

ArticleAmerican journal of physiology. Renal physiology2015

Hyperglycemia in the absence of cilia accelerates cystogenesis and induces renal damage.

Kelli M Sas, Hong Yin, Wayne R Fitzgibbon, Catalin F Baicu, Michael R Zile, Stacy L Steele, May Amria, Takamitsu Saigusa, Jason Funk, Marlene A Bunni and 4 more

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 16% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 21 citations in OpenAlex.

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  12. Truncating PKHD1 and PKD2 mutations alter energy metabolism.American journal of physiology. Renal physiology · 2019
    Article
  13. Article
  14. Environmental hit on a genetic basis in polycystic kidney disease.American journal of physiology. Renal physiology · 2016
    Article
  15. Glucose promotes secretion-dependent renal cyst growth.Journal of molecular medicine (Berlin, Germany) · 2016
    Article
  16. Suppressing angiotensinogen synthesis attenuates kidney cyst formation in a Pkd1 mouse model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 1 country.

Kelli M SasDivision of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina; sask@med.umich.edu.
Hong YinDepartment of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio;
Wayne R FitzgibbonDivision of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina;
Catalin F BaicuDivision of Cardiology, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina;
Michael R ZileRalph H. Johnson Veterans Administration Medical Center, Charleston, South Carolina; Division of Cardiology, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina;
Stacy L SteeleRalph H. Johnson Veterans Administration Medical Center, Charleston, South Carolina; Division of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina;
May AmriaDivision of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina;
Takamitsu SaigusaDivision of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina;
Jason FunkDivision of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina;
Marlene A BunniDivision of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina;
Gene P SiegalDepartment of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, Alabama; and Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama.
Brian J SirokyDepartment of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio;
John J BisslerDepartment of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio;
P Darwin BellRalph H. Johnson Veterans Administration Medical Center, Charleston, South Carolina; Division of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina;
Medical University of South Carolina · USCincinnati Children's Hospital Medical Center · USRalph H. Johnson VA Medical Center · USUniversity of Alabama at Birmingham · US

Funding

UAB Recessive PKD Research and Translational Core CenterP30DK074038 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YODER, BRADLEY K. · 2005 to 2019
$16.6M
CELLULAR MECHANISMS--TUBULOGLOMERULAR FEEDBACK SYSTEMR01DK032032 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BELL, PHILLIP DARWIN · 1986 to 2009
$2.5M
Training Grant in Renal Function and DiseaseT32DK007752 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BELL, PHILLIP DARWIN · 1998 to 2013
$1.5M
Modifiers of Cyst Progression in Polycystic Kidney DiseaseI01BX002007 · VA · RALPH H JOHNSON VA MEDICAL CENTER · PI BELL, PHILLIP DARWIN · 2013 to 2016
–
BLRD VA I01 BX002007NIDDK NIH HHS DK-32032NIDDK NIH HHS P30 DK-074038NIDDK NIH HHS P30 DK074038NIDDK NIH HHS T32 DK007752
6 · The paper itself

Abstract

In polycystic kidney disease (PKD), the rate of cyst formation and disease progression is highly variable. The lack of predictability in disease progression may be due to additional environmental factors or pathophysiological processes called "third hits." Diabetes is a growing epidemic, and recent studies suggest that PKD patients may be at an increased risk for this disease. We sought to determine if hyperglycemia enhances the initiation and rate of cystogenesis. Tamoxifen was administered to adult Ift88 conditional floxed allele mice to induce cilia loss in the presence of Cre. Subsequent administration of streptozotocin resulted in equivalent hyperglycemia in cilia(+) and cilia(-) mice. Hyperglycemia with loss of cilia increased the rate of cyst formation and cell proliferation. Structural and functional alterations in the kidney, including focal glomerular foot process effacement, interstitial inflammation, formation of primitive renal tubules, polyuria, and increased proteinuria, were also observed in hyperglycemic cilia(-) mice. Gene array analysis indicated enhanced Wnt and epithelial-to-mesenchymal transition signaling in the kidney of hyperglycemic cilia(-) mice. These data show that hyperglycemia, in the absence of cilia, results in renal structural and functional damage and accelerates cystogenesis, suggesting that diabetes is a risk factor in the progression of PKD.

Indexed as

AnimalsCell ProliferationEpithelial-Mesenchymal TransitionFemaleHemodynamicsHyperglycemiaKidneyKidney Function TestsMaleMice, KnockoutPolycystic Kidney DiseasesRandom AllocationWnt ProteinsWnt Proteinsdiabetesepithelial-to-mesenchymal transitionpolycystic kidney diseasestreptozotocinWnt

Identifiers

PMID25904703
PMCPMC4490377
OpenAlexW1976038876

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.