Evidence map›Paper›PMID 19454727›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2009

Poly(ADP-ribose) polymerase-1 regulates the progression of autoimmune nephritis in males by inducing necrotic cell death and modulating inflammation.

Neelakshi R Jog, Joudy-Ann Dinnall, Stefania Gallucci, Michael P Madaio, Roberto Caricchio

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
1.3field-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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Article
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  17. Article
  18. HMGB1 in health and disease.Molecular aspects of medicine · 2014
    Review
  19. Article
  20. Review
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 4 institutions in 1 country.

Neelakshi R JogDepartment of Medicine, Division of Rheumatology, University of Pennsylvania, Philadelphia, PA 19104, USA.
Joudy-Ann Dinnall
Stefania Gallucci
Michael P Madaio
Roberto Caricchio
Children's Hospital of Philadelphia · USAugusta University · USTemple University · USUniversity of Pennsylvania · US

Funding

The role of cell death in Lupus NephritisR01AR061569 · NIAMS · TEMPLE UNIV OF THE COMMONWEALTH · PI CARICCHIO, ROBERTO · 2012 to 2016
$2.3M
SLE AUTOANTIGEN TRAFFICKING AND DISPLAY DURING APOPTOSISK08AR048126 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI CARICCHIO, ROBERTO · 2004 to 2008
$513k
NIAMS NIH HHS K08 AR048126NIAMS NIH HHS R01 AR061569
6 · The paper itself

Abstract

Necrotic lesions and necrotic cell death characterize severe autoimmune nephritides, and contribute to local inflammation and to progression of the disease. Poly(ADP-ribose) polymerase-1 (PARP-1), a DNA repair enzyme, is involved in the induction of necrosis and is a key player in the acute and chronic inflammation. Therefore, we hypothesized that PARP-1 controls the severity of nephritis by mediating the induction of necrosis in the kidney. We used lupus and anti-glomerular basement membrane models of nephritis to determine the effects of PARP-1 on the inflammatory response in the kidney. We show in this study that PARP-1 is indeed activated during the course of glomerulonephritis. We also show that the absence of PARP-1 or its pharmacological inhibition results in milder nephritis, with lower blood urea nitrogen levels, reduced necrotic lesions, and higher survival rates. The relevance of PARP-1 showed a strong male sex specificity, and treatment of male mice with 17beta-estradiol prolonged their survival during the course of nephritis. PARP-1 also regulated TNF-alpha expression and up-regulation of adhesion molecules, further supporting a role of PARP-1 in the inflammatory process within the kidney. Our results demonstrate that PARP-1 activation and consequent necrotic cell death play an important role in the pathogenesis of male nephritis, and suggest that PARP-1 can be a novel therapeutic target in glomerulonephritis.

Indexed as

AnimalsAutoimmune DiseasesDisease ProgressionEstradiolFemaleGlomerulonephritisInflammationKidneyMaleMiceNecrosisPoly(ADP-ribose) PolymerasesSex FactorsSurvival RateEstradiolPoly(ADP-ribose) Polymerases

Identifiers

PMID19454727
PMCPMC4827346
OpenAlexW1488403741

What OpenQuestion holds

Textmetadata
LicenceTDM
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.