Evidence map›Paper›PMID 25825084›Full record

ReviewNature reviews. Nephrology2015

Genetics and pathogenesis of systemic lupus erythematosus and lupus nephritis.

Chandra Mohan, Chaim Putterman

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 187 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
187citing papers in PubMed, 5 pooled it
32.4field-weighted citation impact, top 1% 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

187 citing papers in PubMed, 5 syntheses or guidelines pooled it, 370 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Diet and Systemic Lupus Erythematosus (SLE): From Supplementation to Intervention.International journal of environmental research and public health · 2022
    Pooled it
  4. Pooled it
  5. Fracture risk and bone mineral density levels in patients with systemic lupus erythematosus: a systematic review and meta-analysis.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2016
    Pooled it
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  20. Lupus nephritis.Nature reviews. Disease primers · 2025
    Review

127 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.

Chandra MohanDepartment of Bioengineering, University of Houston, 3605 Cullen Boulevard, Houston, TX 77204, USA.
Chaim PuttermanDivision of Rheumatology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.
Albert Einstein College of Medicine · US

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 AR048692NIDDK NIH HHS DK090319
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disorder that has a broad spectrum of effects on the majority of organs, including the kidneys. Approximately 40-70% of patients with SLE will develop lupus nephritis. Renal assault during SLE is initiated by genes that breach immune tolerance and promote autoantibody production. These genes might act in concert with other genetic factors that augment innate immune signalling and IFN-I production, which in turn can generate an influx of effector leucocytes, inflammatory mediators and autoantibodies into end organs, such as the kidneys. The presence of cognate antigens in the glomerular matrix, together with intrinsic molecular abnormalities in resident renal cells, might further accentuate disease progression. This Review discusses the genetic insights and molecular mechanisms for key pathogenic contributors in SLE and lupus nephritis. We have categorized the genes identified in human studies of SLE into one of four pathogenic events that lead to lupus nephritis. We selected these categories on the basis of the cell types in which these genes are expressed, and the emerging paradigms of SLE pathogenesis arising from murine models. Deciphering the molecular basis of SLE and/or lupus nephritis in each patient will help physicians to tailor specific therapies.

Indexed as

Adaptive ImmunityAnimalsHumansImmune ToleranceInterleukinsLupus Erythematosus, SystemicLupus NephritisProtein Tyrosine Phosphatase, Non-Receptor Type 22src-Family KinasesToll-Like ReceptorsInterleukinsProtein Tyrosine Phosphatase, Non-Receptor Type 22PTPN22 protein, humansrc-Family KinasesToll-Like Receptors

Identifiers

PMID25825084
OpenAlexW1993116843

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.