Evidence map›Paper›PMID 21617121›Full record

ArticleJournal of the American Society of Nephrology : JASN2011

Suramin inhibits renal fibrosis in chronic kidney disease.

Na Liu, Evelyn Tolbert, Maoyin Pang, Murugavel Ponnusamy, Haidong Yan, Shougang Zhuang

Abstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

46 citing papers in PubMed, 80 citations in OpenAlex.

  1. Review
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  13. Critical roles of SMYD2 lysine methyltransferase in mediating renal fibroblast activation and kidney fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
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  18. Review
  19. Targeting STAT3 signaling in kidney disease.American journal of physiology. Renal physiology · 2019
    Review
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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

6 authors at 3 institutions in 2 countries.

Na LiuDepartment of Medicine, Rhode Island Hospital and Brown University School of Medicine, Providence, Rhode Island, USA.
Evelyn Tolbert
Maoyin Pang
Murugavel Ponnusamy
Haidong Yan
Shougang Zhuang
Rhode Island Hospital · USShanghai East Hospital · CNBrown University · US

Funding

Histone deacetylases as novel therapeutic targets for kidney fibrosisR01DK085065 · NIDDK · RHODE ISLAND HOSPITAL · PI ZHUANG, SHOUGANG · 2010 to 2017
$2.8M
Dedifferentiation Following Renal Cell InjuryR01DK071997 · NIDDK · RHODE ISLAND HOSPITAL · PI ZHUANG, SHOUGANG · 2006 to 2009
$1.1M
NIDDK NIH HHS DK-071997NIDDK NIH HHS DK-085065NIDDK NIH HHS R01 DK071997NIDDK NIH HHS R01 DK085065
6 · The paper itself

Abstract

The activation of cytokine and growth factor receptors associates with the development and progression of renal fibrosis. Suramin is a compound that inhibits the interaction of several cytokines and growth factors with their receptors, but whether suramin inhibits the progression of renal fibrosis is unknown. Here, treatment of cultured renal interstitial fibroblasts with suramin inhibited their activation induced by TGF-β1 and serum. In a mouse model of obstructive nephropathy, administration of a single dose of suramin immediately after ureteral obstruction abolished the expression of fibronectin, largely suppressed expression of α-SMA and type I collagen, and reduced the deposition of extracellular matrix proteins. Suramin also decreased the expression of multiple cytokines including TGF-β1 and reduced the interstitial infiltration of leukocytes. Moreover, suramin decreased expression of the type II TGF-β receptor, blocked phosphorylation of the EGF and PDGF receptors, and inactivated several signaling pathways associated with the progression of renal fibrosis. In a rat model of CKD, suramin abrogated proteinuria, limited the decline of renal function, and prevented glomerular and tubulointerstitial damage. Collectively, these findings indicate that suramin is a potent antifibrotic agent that may have therapeutic potential for patients with fibrotic kidney diseases.

Indexed as

Disease ProgressionActinsAnimalsAntineoplastic AgentsCells, CulturedChronic DiseaseDisease Models, AnimalFibroblastsFibronectinsFibrosisKidneyKidney DiseasesMaleMiceMice, Inbred C57BLProteinuriaActinsAntineoplastic AgentsFibronectinsSmad ProteinsSuraminTransforming Growth Factor beta1

Identifiers

PMID21617121
PMCPMC3103726
OpenAlexW2157318371

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.