Evidence map›Paper›PMID 17287345›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2007

Amelioration of progressive renal injury by genetic manipulation of Klotho gene.

Yoshisuke Haruna, Naoki Kashihara, Minoru Satoh, Naruya Tomita, Tamehachi Namikoshi, Tamaki Sasaki, Toshihiko Fujimori, Ping Xie, Yashpal S Kanwar

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed, 2 pooled it
6.0field-weighted citation impact, top 4% 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

133 citing papers in PubMed, 2 syntheses or guidelines pooled it, 246 citations in OpenAlex.

  1. Pooled it
  2. Correlation between SolubleBioMed research international · 2018
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  19. PKC regulates αKlotho gene expression in MDCK and NRK-52E cells.Pflugers Archiv : European journal of physiology · 2024
    Article
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73 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 2 countries.

Yoshisuke HarunaDivision of Nephrology, Department of Internal Medicine, Kawasaki Medical School, Kurashiki, Okayama 701-0192, Japan.
Naoki Kashihara
Minoru Satoh
Naruya Tomita
Tamehachi Namikoshi
Tamaki Sasaki
Toshihiko Fujimori
Ping Xie
Yashpal S Kanwar
Kawasaki Medical School · JPNorthwestern University · USKyoto University · JP

Funding

Pathogenesis of Diabetic NephropathyR01DK060635 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI QUAGGIN, SUSAN E. · 2002 to 2023
$6.6M
GLOMERULAR CAPILLARY WALL: NORMAL AND PATHOLOGICR01DK028492 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI KANWAR, YASHPAL S. · 1986 to 2008
$1.9M
GLOMERULAR CAPILLARY WALL--NORMAL AND PATHOLOGICR37DK028492 · NIDDK · NORTHWESTERN UNIVERSITY · PI KANWAR, YASHPAL S. · 1998 to 2003
$1.2M
NIDDK NIH HHS DK28492NIDDK NIH HHS DK60635NIDDK NIH HHS R01 DK028492NIDDK NIH HHS R01 DK060635NIDDK NIH HHS R37 DK028492
6 · The paper itself

Abstract

Klotho, an antiaging gene with restricted organ distribution, is mainly expressed in the kidney tubules; the mutant mice have shortened life span, arteriosclerosis, anemia, and osteoporesis, features common to patients with chronic renal failure. Conceivably, the reduction of the Klotho gene expression may contribute to the development of kidney failure; alternatively, its overexpression may lead to the amelioration of renal injury in an ICR-derived glomerulonephritis (ICGN) mouse model with subtle immune complex-mediated disease. To address this issue, four different strains of mice were generated by cross-breeding: ICGN mice without the Klotho transgene (ICGN), ICGN mice with the Klotho transgene (ICGN/klTG), wild-type mice with the Klotho transgene (klTG), and wild-type mice without the Klotho transgene (control). At 40 weeks old, the survival rate was approximately 30% in ICGN mice, and approximately 70% in the ICGN/klTG group. This improvement was associated with dramatic improvement in renal functions, morphological lesions, and cytochrome c oxidase activity but a reduction in beta-galactosidase activity (a senescence-associated protein), mitochondrial DNA fragmentation, superoxide anion generation, lipid peroxidation, and Bax protein expression and apoptosis. Interestingly, improvement was seen in both the tubular and glomerular compartments of the kidney, although Klotho is exclusively confined to the tubules, suggesting that its gene product has a remarkable renoprotective effect by potentially serving as a circulating hormone while mitigating the mitochondrial oxidative stress.

Indexed as

AnimalsDisease ProgressionGene Expression RegulationGenetic TherapyGlucuronidaseKidney DiseasesKlotho ProteinsMiceMice, Inbred StrainsMitochondriaNephronsOxidative StressSurvival RateTissue DistributionTransgenesGlucuronidaseKlotho Proteins

Identifiers

PMID17287345
PMCPMC1892974
OpenAlexW1995746533

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.