Evidence map›Paper›PMID 10859350›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2000

Long-term prevention of renal insufficiency, excess matrix gene expression, and glomerular mesangial matrix expansion by treatment with monoclonal antitransforming growth factor-beta antibody in db/db diabetic mice.

F N Ziyadeh, B B Hoffman, D C Han, M C Iglesias-De La Cruz, S W Hong, M Isono, S Chen, T A McGowan, K Sharma

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

Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 301 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
301citing papers in PubMed, 5 pooled it
35.8field-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

301 citing papers in PubMed, 5 syntheses or guidelines pooled it, 909 citations in OpenAlex.

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  6. Anti-TGF-Journal of the American Society of Nephrology : JASN · 2017
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241 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

F N ZiyadehRenal-Electrolyte and Hypertension Division, University of Pennsylvania, Philadelphia, PA 19104-6144, USA. ziyadeh@mail.med.upenn.edu
B B Hoffman
D C Han
M C Iglesias-De La Cruz
S W Hong
M Isono
S Chen
T A McGowan
K Sharma
University of Pennsylvania · USThomas Jefferson University · US

Funding

Training in Renal ResearchT32DK007006 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI HOLZMAN, LAWRENCE B. · 1986 to 2023
$8.5M
TUBULOINTERSTITIAL KIDNEY CELLS &REPONSE TO GLUCOSER01DK044513 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI CHEN, SHELDON · 1992 to 2009
$2.0M
AMADORI-MODIFIED ALBUMIN IN DIABETIC NEPHROPATHYR01DK054608 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI ZIYADEH, FUAD N · 1998 to 2002
$745k
NIDDK NIH HHS DK-44513NIDDK NIH HHS DK-45193NIDDK NIH HHS DK-54608NIDDK NIH HHS R01 DK044513NIDDK NIH HHS T32 DK007006
6 · The paper itself

Abstract

Emerging evidence suggests that transforming growth factor-beta (TGF-beta) is an important mediator of diabetic nephropathy. We showed previously that short-term treatment with a neutralizing monoclonal anti-TGF-beta antibody (alphaT) in streptozotocin-diabetic mice prevents early changes of renal hypertrophy and increased matrix mRNA. To establish that overactivity of the renal TGF-beta system mediates the functional and structural changes of the more advanced stages of nephropathy, we tested whether chronic administration of alphaT prevents renal insufficiency and glomerulosclerosis in the db/db mouse, a model of type 2 diabetes that develops overt nephropathy. Diabetic db/db mice and nondiabetic db/m littermates were treated intraperitoneally with alphaT or control IgG, 300 microgram three times per week for 8 wk. Treatment with alphaT, but not with IgG, significantly decreased the plasma TGF-beta1 concentration without decreasing the plasma glucose concentration. The IgG-treated db/db mice developed albuminuria, renal insufficiency, and glomerular mesangial matrix expansion associated with increased renal mRNAs encoding alpha1(IV) collagen and fibronectin. On the other hand, treatment with alphaT completely prevented the increase in plasma creatinine concentration, the decrease in urinary creatinine clearance, and the expansion of mesangial matrix in db/db mice. The increase in renal matrix mRNAs was substantially attenuated, but the excretion of urinary albumin factored for creatinine clearance was not significantly affected by alphaT treatment. We conclude that chronic inhibition of the biologic actions of TGF-beta with a neutralizing monoclonal antibody in db/db mice prevents the glomerulosclerosis and renal insufficiency resulting from type 2 diabetes.

Indexed as

Receptors, Cell SurfaceAnimalsAntibodies, MonoclonalCarrier ProteinsDiabetes Mellitus, Type 2Disease Models, AnimalExtracellular MatrixExtracellular Matrix ProteinsGlomerular MesangiumMiceMice, Mutant StrainsProtein Serine-Threonine KinasesReceptors, LeptinReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IIRenal InsufficiencyAntibodies, MonoclonalCarrier ProteinsExtracellular Matrix ProteinsProtein Serine-Threonine KinasesReceptors, Cell SurfaceReceptors, LeptinReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IITransforming Growth Factor beta

Identifiers

PMID10859350
PMCPMC16662
OpenAlexW2165325650

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.