Evidence map›Paper›PMID 19875815›Full record

ArticleJournal of the American Society of Nephrology : JASN2010

Renal dendritic cells ameliorate nephrotoxic acute kidney injury.

Raghu K Tadagavadi, W Brian Reeves

Abstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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

94 citing papers in PubMed, 1 synthesis or guideline pooled it, 152 citations in OpenAlex.

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  15. Selective depletion of a CD64-expressing phagocyte subset mediates protection against toxic kidney injury and failure.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  16. Mired in the glomeruli: witnessing live neutrophil recruitment in the kidney.American journal of physiology. Cell physiology · 2021
    Review
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34 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

2 authors at 1 institution in 1 country.

Raghu K TadagavadiDepartment of Biochemistry and Molecular Biology, Penn State University College of Medicine, Hershey, Pennsylvania, PA, USA.
W Brian Reeves
Lebanon VA Medical Center · US

Funding

Epithelial/Dendritic Cell Cross-Talk in Acute Kidney InjuryR01DK081876 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI REEVES, WILLIAM BRIAN · 2009 to 2015
$2.4M
Tumor necrosis factor in cisplatin nephrotoxicityR01DK063120 · NIDDK · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI REEVES, WILLIAM BRIAN · 2004 to 2008
$1.4M
NIDDK NIH HHS R01 DK063120NIDDK NIH HHS R01 DK081876NIDDK NIH HHS R01DK63120
6 · The paper itself

Abstract

Inflammation contributes to the pathogenesis of acute kidney injury. Dendritic cells (DCs) are immune sentinels with the ability to induce immunity or tolerance, but whether they mediate acute kidney injury is unknown. Here, we studied the distribution of DCs within the kidney and the role of DCs in cisplatin-induced acute kidney injury using a mouse model in which DCs express both green fluorescence protein and the diphtheria toxin receptor. DCs were present throughout the tubulointerstitium but not in glomeruli. We used diphtheria toxin to deplete DCs to study their functional significance in cisplatin nephrotoxicity. Mice depleted of DCs before or coincident with cisplatin treatment but not at later stages experienced more severe renal dysfunction, tubular injury, neutrophil infiltration and greater mortality than nondepleted mice. We used bone marrow chimeric mice to confirm that the depletion of CD11c-expressing hematopoietic cells was responsible for the enhanced renal injury. Finally, mixed bone marrow chimeras demonstrated that the worsening of cisplatin nephrotoxicity in DC-depleted mice was not a result of the dying or dead DCs themselves. After cisplatin treatment, expression of MHC class II decreased and expression of inducible co-stimulator ligand increased on renal DCs. These data demonstrate that resident DCs reduce cisplatin nephrotoxicity and its associated inflammation.

Indexed as

Acute Kidney InjuryAnimalsApoptosisBone MarrowCD11c AntigenCisplatinDendritic CellsDisease Models, AnimalGreen Fluorescent ProteinsHeparin-binding EGF-like Growth FactorIntercellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLMice, TransgenicNephronsCD11c AntigenCisplatinGreen Fluorescent ProteinsHbegf protein, mouseHeparin-binding EGF-like Growth FactorIntercellular Signaling Peptides and Proteins

Identifiers

PMID19875815
PMCPMC2799272
OpenAlexW2136049487

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.