Evidence map›Paper›PMID 24493870›Full record

ReviewNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association2014

TWEAK and the progression of renal disease: clinical translation.

Ana B Sanz, M Concepcion Izquierdo, Maria Dolores Sanchez-Niño, Alvaro C Ucero, Jesus Egido, Marta Ruiz-Ortega, Adrián Mario Ramos, Chaim Putterman, Alberto Ortiz

Open access · greenAbstract readReview
In one paragraph

Review in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

51 citing papers in PubMed, 111 citations in OpenAlex.

  1. Trial
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  9. Review
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  14. New biomarkers in SLE: from bench to bedside.Rheumatology (Oxford, England) · 2020
    Review
  15. Article
  16. Article
  17. Acute Kidney Injury in Children after Hematopoietic Cell Transplantation Is Associated with Elevated Urine CXCL10 and CXCL9.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2020
    Observational
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  19. 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 4 institutions in 2 countries.

Ana B SanzDialysis Unit, IIS-Fundacion Jimenez Diaz, Madrid, Spain.
M Concepcion Izquierdo
Maria Dolores Sanchez-Niño
Alvaro C Ucero
Jesus Egido
Marta Ruiz-Ortega
Adrián Mario Ramos
Chaim Putterman
Alberto Ortiz
Hospital Universitario Fundación Jiménez Díaz · ESUniversidad Autónoma de Madrid · ESAlbert Einstein College of Medicine · USSpanish Clinical Research Network · ES

Funding

The Renal Pathogenicity of anti-DNA AntibodiesR01AR048692 · NIAMS · YESHIVA UNIVERSITY · PI PUTTERMAN, CHAIM · 2002 to 2013
$4.0M
TNF-like weak inducer of apoptosis (TWEAK) signaling in lupus nephritisR01DK090319 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI PUTTERMAN, CHAIM · 2011 to 2014
$1.5M
The Renal Pathogenicity of Anti-DNA AntibodiesR56AR048692 · NIAMS · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI PUTTERMAN, CHAIM · 2008 to 2008
$365k
NIAMS NIH HHS AR048692NIAMS NIH HHS R01 AR048692NIAMS NIH HHS R56 AR048692NIDDK NIH HHS DK090319NIDDK NIH HHS R01 DK090319
6 · The paper itself

Abstract

Tumour necrosis factor-like weak inducer of apoptosis (TWEAK) activates the fibroblast growth factor-inducible-14 (Fn14) receptor. TWEAK has actions on intrinsic kidney cells and on inflammatory cells of potential pathophysiological relevance. The effects of TWEAK in tubular cells have been explored in most detail. In cultured murine tubular cells TWEAK induces the expression of inflammatory cytokines, downregulates the expression of Klotho, is mitogenic, and in the presence of sensitizing agents promotes apoptosis. Similar actions were observed on glomerular mesangial cells. In vivo TWEAK actions on healthy kidneys mimic cell culture observations. Increased expression of TWEAK and Fn14 was reported in human and experimental acute and chronic kidney injury. The role of TWEAK/Fn14 in kidney injury has been demonstrated in non-inflammatory compensatory renal growth, acute kidney injury and chronic kidney disease of immune and non-immune origin, including hyperlipidaemic nephropathy, lupus nephritis (LN) and anti-GBM nephritis. The nephroprotective effect of TWEAK or Fn14 targeting in immune-mediated kidney injury is the result of protection from TWEAK-induced injury of renal intrinsic cells, not from interference with the immune response. A phase I dose-ranging clinical trial demonstrated the safety of anti-TWEAK antibodies in humans. A phase II randomized placebo-controlled clinical trial exploring the efficacy, safety and tolerability of neutralizing anti-TWEAK antibodies as a tissue protection strategy in LN is ongoing. The eventual success of this trial may expand the range of kidney diseases in which TWEAK targeting should be explored.

Indexed as

ApoptosisTranslational Research, BiomedicalAnimalsCytokine TWEAKDisease ProgressionHumansKidney DiseasesMiceTumor Necrosis FactorsCytokine TWEAKTNFSF12 protein, humanTnfsf12 protein, mouseTumor Necrosis Factorsapoptosisclinical trialsfibrosisinflammationnecroptosisproteinuria

Identifiers

PMID24493870
PMCPMC3968810
OpenAlexW2135800410

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.