Evidence map›Paper›PMID 16159900›Full record

ReviewAmerican journal of physiology. Renal physiology2005

Experimental membranous nephropathy redux.

Andrey V Cybulsky, Richard J Quigg, David J Salant

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Renal physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

58 citing papers in PubMed, 124 citations in OpenAlex.

  1. Effects of rituximab on morphofunctional abnormalities of membranous glomerulopathy.Clinical journal of the American Society of Nephrology : CJASN · 2008
    Trial
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  19. Unmet challenges in membranous nephropathy.Current opinion in nephrology and hypertension · 2019
    Review
  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

3 authors at 1 institution in 1 country.

Andrey V CybulskyRenal Section, EBRC 504, Boston Univ. Medical Ctr., 650 Albany St., Boston, MA 02118, USA.
Richard J Quigg
David J Salant
Boston Medical Center · US

Funding

RESEARCH TRAINING IN NEPHROLOGYT32DK007053 · NIDDK · BOSTON UNIVERSITY MEDICAL CAMPUS · PI RIFKIN, IAN R · 1986 to 2019
$3.9M
MEDIATION OF ANTIBODY-INDUCED GLOMERULAR INJURYR01DK030932 · NIDDK · BOSTON UNIVERSITY MEDICAL CENTER HOSP · PI SALANT, DAVID J · 1986 to 2010
$3.4M
Role of the Complement System in Renal DiseaseR01DK041873 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI QUIGG, RICHARD J. · 1994 to 2011
$3.4M
Identification of The Membranous Nephropathy AntigenR21DK067658 · NIDDK · BOSTON MEDICAL CENTER · PI SALANT, DAVID J · 2004 to 2005
$443k
Antibody Mediated Glomerular InjuryR56DK030932 · NIDDK · BOSTON MEDICAL CENTER · PI SALANT, DAVID J · 2005 to 2005
$81k
Role of the complement system in renal diseaseR56DK041873 · NIDDK · UNIVERSITY OF CHICAGO · PI QUIGG, RICHARD J · 2006 to 2006
$75k
COMPLEMENT ACTIVATION OF THE GLOMERULER EPITHELIAL CELLR29DK041873 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI QUIGG, RICHARD J · 1989 to 1993
–
NIDDK NIH HHS DK-067658NIDDK NIH HHS DK-30932NIDDK NIH HHS DK-41873NIDDK NIH HHS R01 DK030932NIDDK NIH HHS R01 DK041873NIDDK NIH HHS R21 DK067658NIDDK NIH HHS R56 DK030932NIDDK NIH HHS R56 DK041873NIDDK NIH HHS T32 DK007053
6 · The paper itself

Abstract

Membranous nephropathy (MN) is a common cause of nephrotic syndrome in adults. Active and passive Heymann nephritis (HN) in rats are valuable experimental models because their features so closely resemble human MN. In HN, subepithelial immune deposits form in situ as a result of circulating antibodies. Complement activation leads to assembly of C5b-9 on glomerular epithelial cell (GEC) plasma membranes and is essential for sublethal GEC injury and the onset of proteinuria. This review revisits HN and focuses on areas of substantial progress in recent years. The response of the GEC to sublethal C5b-9 attack is not simply due to disruption of the plasma membrane but is due to the activation of specific signaling pathways. These include activation of protein kinases, phospholipases, cyclooxygenases, transcription factors, growth factors, NADPH oxidase, stress proteins, proteinases, and others. Ultimately, these signals impact on cell metabolic pathways and the structure/function of lipids and key proteins in the cytoskeleton and slit-diaphragm. Some signals affect GEC adversely. Thus C5b-9 induces partial dissolution of the actin cytoskeleton. There is a decline in nephrin expression, reduction in F-actin-bound nephrin, and loss of slit-diaphragm integrity. Other signals, such as endoplasmic reticulum stress, may limit complement-induced injury, or promote recovery. The extent of complement activation and GEC injury is dependent, in part, on complement-regulatory proteins, which act at early or late steps within the complement cascade. Identification of key steps in complement activation, the cellular signaling pathways, and the targets will facilitate therapeutic intervention in reversing GEC injury in human MN.

Indexed as

AnimalsComplement Membrane Attack ComplexGene Expression RegulationGlomerulonephritis, MembranousHumansRatsSignal TransductionComplement Membrane Attack Complex

Identifiers

PMID16159900
PMCPMC1325222
OpenAlexW2055761277

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.