Evidence map›Paper›PMID 25820160›Full record

ArticleEuropean journal of pharmacology2015

Chelation of dietary iron prevents iron accumulation and macrophage infiltration in the type I diabetic kidney.

Tatsuyori Morita, Daisuke Nakano, Kento Kitada, Satoshi Morimoto, Atsuhiro Ichihara, Hirofumi Hitomi, Hiroyuki Kobori, Ichiro Shiojima, Akira Nishiyama

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

Article in European journal of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. The Role of Renal Cell Senescence in Diabetic Kidney Disease: Mechanisms and Therapeutic Advances.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
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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 2 institutions in 1 country.

Tatsuyori MoritaDepartment of Pharmacology, Kagawa University, 1750-1 Miki, Kita, Kagawa, Japan; The Second Department of Internal Medicine, Kansai Medical University, Japan.
Daisuke NakanoDepartment of Pharmacology, Kagawa University, 1750-1 Miki, Kita, Kagawa, Japan. Electronic address: dnakano@med.kagawa-u.ac.jp.
Kento KitadaDepartment of Pharmacology, Kagawa University, 1750-1 Miki, Kita, Kagawa, Japan.
Satoshi MorimotoDepartment of Endocrinology and Hypertension, Tokyo Women's Medical University, Tokyo, Japan.
Atsuhiro IchiharaDepartment of Endocrinology and Hypertension, Tokyo Women's Medical University, Tokyo, Japan.
Hirofumi HitomiDepartment of Pharmacology, Kagawa University, 1750-1 Miki, Kita, Kagawa, Japan.
Hiroyuki KoboriDepartment of Pharmacology, Kagawa University, 1750-1 Miki, Kita, Kagawa, Japan.
Ichiro ShiojimaDepartment of Endocrinology and Hypertension, Tokyo Women's Medical University, Tokyo, Japan.
Akira NishiyamaDepartment of Pharmacology, Kagawa University, 1750-1 Miki, Kita, Kagawa, Japan.
Kagawa University · JPTokyo Women's Medical University · JP

Funding

Intrarenal Augmentation of Angiotensinogen by Ang IIR01DK072408 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI NAVAR, LUIS GABRIEL · 2006 to 2010
$1.2M
NIDDK NIH HHS R01 DK072408
6 · The paper itself

Abstract

We previously reported that the functional deletion of p21, a cyclin-dependent kinase inhibitor, in mice attenuated renal cell senescence in streptozotocin (STZ)-induced type 1 diabetic mice. In the present study, we investigated the effect of iron chelation on renal cell senescence and inflammation in the type 1 diabetic kidney. STZ-treated mice showed increase in iron accumulation, tubular cell senescence and macrophage infiltration at week 28 in the kidney. Administering deferasirox, which removes only dietary iron, significantly attenuated iron accumulation in proximal tubules and the number of infiltrating F4/80-positive cells without effecting blood glucose, hematocrit or hemoglobin levels. In contrast however, deferasirox did not influence renal cell senescence. The lack of p21 decreased the renal tubular iron accumulation and did not change tubular cell senescence. Interestingly, the STZ-treated animals showed an increase in p16, another cyclin-dependent kinase inhibitor. The results suggest that type 1 diabetes increases renal tubular iron accumulation and macrophage infiltration through a p21-dependent mechanism, and that the chelation of dietary iron attenuates these responses.

Indexed as

Iron, DietaryAnimalsBenzoatesCellular SenescenceCyclin-Dependent Kinase Inhibitor p21DeferasiroxDiabetes Mellitus, Type 1Diabetic NephropathiesGene Knockout TechniquesIronIron Chelating AgentsKidneyMacrophagesMaleMiceMice, Inbred C57BLBenzoatesCyclin-Dependent Kinase Inhibitor p21DeferasiroxIronIron Chelating AgentsIron, DietaryTriazolesCellular senescenceDiabetic nephropathyIronP21Proximal tubular cells

Identifiers

PMID25820160
PMCPMC4423393
OpenAlexW2029355900

What OpenQuestion holds

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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.