Evidence map›Paper›PMID 26914452›Full record

ArticlePloS one2016

Phosphate-Induced Renal Fibrosis Requires the Prolyl Isomerase Pin1.

Zhong-Jian Shen, Jie Hu, Kazuhiro Shiizaki, Makoto Kuro-o, James S Malter

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. The effects of elevated phosphate on the kidney - damaging the gatekeeper.Pflugers Archiv : European journal of physiology · 2026
    Review
  3. Review
  4. Review
  5. Article
  6. The molecular mechanisms of peptidyl-prolylFrontiers in pharmacology · 2024
    Review
  7. Article
  8. Phosphate and Cellular Senescence.Advances in experimental medicine and biology · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Cisplatin nephrotoxicity as a model of chronic kidney disease.Laboratory investigation; a journal of technical methods and pathology · 2018
    Article
  15. Article
  16. Article
  17. 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

5 authors at 1 institution in 1 country.

Zhong-Jian ShenDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America.
Jie HuDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America.
Kazuhiro ShiizakiDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America.
Makoto Kuro-oDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America.
James S MalterDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America.
The University of Texas Southwestern Medical Center · US

Funding

Thr Role of Pin1 in AirwayP01HL088594 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI JARJOUR, NIZAR N · 2008 to 2017
$21.0M
NHLBI NIH HHS P01 HL088594NHLBI NIH HHS P01HL088594
6 · The paper itself

Abstract

Tubulo-interstitial fibrosis is a common, destructive endpoint for a variety of kidney diseases. Fibrosis is well correlated with the loss of kidney function in both humans and rodents. The identification of modulators of fibrosis could provide novel therapeutic approaches to reducing disease progression or severity. Here, we show that the peptidyl-prolyl isomerase Pin1 is an important molecular contributor that facilitates renal fibrosis in a well-characterized animal model. While wild-type mice fed a high phosphate diet (HPD) for 8-12 weeks developed calcium deposition, macrophage infiltration and extracellular matrix (ECM) accumulation in the kidney interstitium, Pin1 null mice showed significantly less pathology. The serum Pi in both WT and KO mice were significantly increased by the HPD, but the serum Ca was slightly decreased in KO compared to WT. In addition, both WT and KO HPD mice had less weight gain but exhibited normal organ mass (kidney, lung, spleen, liver and heart). Unexpectedly, renal function was not initially impaired in either genotype irrespective of the HPD. Our results suggest that diet containing high Pi induces rapid renal fibrosis before a significant impact on renal function and that Pin1 plays an important role in the fibrotic process.

Indexed as

AnimalsCalciumDietDisease Models, AnimalDisease ProgressionExtracellular MatrixFibrosisKidneyKidney DiseasesMacrophage ActivationMiceMice, Inbred C57BLMice, KnockoutNIMA-Interacting Peptidylprolyl IsomerasePeptidylprolyl IsomerasePhosphatesCalciumNIMA-Interacting Peptidylprolyl IsomerasePeptidylprolyl IsomerasePhosphatesPIN1 protein, humanPin1 protein, mouse

Identifiers

PMID26914452
PMCPMC4767802
OpenAlexW2276937735

What OpenQuestion holds

Textmetadata
LicenceCC0
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.