Evidence map›Paper›PMID 18216320›Full record

ArticleJournal of the American Society of Nephrology : JASN2008

Latent TGF-beta1 protects against crescentic glomerulonephritis.

Xiao R Huang, Arthur C K Chung, Li Zhou, Xiao J Wang, Hui Y Lan

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 5% 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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.

  1. Association ofFrontiers in genetics · 2020
    Pooled it
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  18. RIPK3: A New Player in Renal Fibrosis.Frontiers in cell and developmental biology · 2020
    Review
  19. Transforming Growth Factor-Beta1 in Diabetic Kidney Disease.Frontiers in cell and developmental biology · 2020
    Review
  20. Diverse Role of TGF-β in Kidney Disease.Frontiers in cell and developmental biology · 2020
    Review

6 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

5 authors at 3 institutions in 3 countries.

Xiao R HuangDepartment of Medicine, The University of Hong Kong Li Ka Shing Faculty of Medicine, Hong Kong, China.
Arthur C K Chung
Li Zhou
Xiao J Wang
Hui Y Lan
Chinese University of Hong Kong · CNOregon Health & Science University · USUniversity of Hong Kong · HK

Funding

TGF BETA SIGNALING AND SKIN CARCINOGENESISR01CA079998 · NCI · UNIVERSITY OF COLORADO DENVER · PI WANG, XIAO-JING · 1999 to 2009
$2.1M
Effects of altering TGF beta signaling on wound healingR01GM070966 · NIGMS · OREGON HEALTH & SCIENCE UNIVERSITY · PI WANG, XIAO-JING · 2004 to 2007
$940k
NCI NIH HHS CA79998NCI NIH HHS R01 CA079998NIGMS NIH HHS GM70966NIGMS NIH HHS R01 GM070966
6 · The paper itself

Abstract

Despite the critical role that TGF-beta plays in renal fibrosis, transgenic mice that overexpress human latent TGF-beta1 in the skin exhibit normal renal histology and function even though circulating levels of latent TGF-beta1 are an order of magnitude higher than wild-type animals. In fact, latent TGF-beta1 seems to protect against renal inflammation in a model of ureteral obstruction. It is unknown, however, whether latent TGF-beta1 also has this effect in immunologically mediated forms of renal disease such as anti-GBM crescentic glomerulonephritis. We induced anti-GBM disease in wild-type and transgenic mice overexpressing latent TGF-beta1 in keratinocytes. After 14 days, wild-type mice developed progressive crescentic glomerulonephritis with severe renal inflammation and fibrosis. In transgenic mice, proteinuria was reduced by 50%, renal function was preserved, and the formation of glomerular crescents was suppressed by 70%. In addition, transgenic animals had reduced renal inflammation, evidenced by a 70% decrease in the accumulation of T cells and macrophages, and reduced expression of renal IL-1beta, TNFalpha, and MCP-1 by 70 to 80%. Progressive renal fibrosis was also prevented in the transgenic mice, and these protective effects were associated with elevated levels of latent, but not active, TGF-beta1 in plasma and renal tissue. Renal Smad7 was up-regulated and both NF-kappaB and TGF-beta/Smad2/3 activation were suppressed. In conclusion, mice overexpressing latent TGF-beta1 in the skin were protected against anti-GBM crescentic glomerulonephritis, possibly via Smad 7-mediated inhibition of NF-kappaB-dependent renal inflammation and TGF-beta/Smad2/3-dependent fibrosis.

Indexed as

AnimalsChemokine CCL2Complement System ProteinsDisease Models, AnimalFibrosisGlomerular Basement MembraneGlomerulonephritisHumansKeratinocytesMacrophagesMiceMice, Inbred ICRMice, TransgenicProteinuriaSmad2 ProteinSmad3 ProteinCcl2 protein, mouseChemokine CCL2Complement System ProteinsSmad2 ProteinSmad2 protein, mouseSmad3 ProteinSmad3 protein, mouseSmad7 ProteinSmad7 protein, mouseTranscription Factor RelATransforming Growth Factor beta1Tumor Necrosis Factor-alpha

Identifiers

PMID18216320
PMCPMC2396747
OpenAlexW2158118120

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.