Evidence map›Paper›PMID 30455396›Full record

ArticleBioscience reports2018

Galectin 3 inhibition attenuates renal injury progression in cisplatin-induced nephrotoxicity.

Hong-Yan Li, Shen Yang, Jing-Chun Li, Jian-Xun Feng

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 41 citations in OpenAlex.

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  19. Letter to the Editor: Not all modified citrus pectins are the same: size does matter.American journal of physiology. Heart and circulatory physiology · 2019
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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

4 authors at 2 institutions in 1 country.

Hong-Yan LiDivision of Nephrology, Huadu District People's Hospital of Guangzhou, Southern Medical University, Guangzhou 510800, P.R. China (lihy0726@126.com (fengjx9101@126.com.ORCID 0000-0002-3307-4028
Shen YangDivision of Nephrology, Huadu District People's Hospital of Guangzhou, Southern Medical University, Guangzhou 510800, P.R. China.
Jing-Chun LiDivision of Nephrology, Huadu District People's Hospital of Guangzhou, Southern Medical University, Guangzhou 510800, P.R. China.
Jian-Xun FengDivision of Nephrology, Xuhui District Centeral Hospital of Shanghai, Shanghai, P.R. China (lihy0726@126.com (fengjx9101@126.com.
Southern Medical University · CNShanghai Xuhui Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nephrotoxicity is a major toxic effect in chemotherapy, which constitutes up to 60% of hospitalized acute kidney injury (AKI). Very few treatment options exist to slow the transition from AKI to subsequent chronic kidney diseases (CKD). Here, we demonstrate that galectin-3 (Gal-3), a β-galactoside binding lectin that plays an important role in kidney fibrosis and renal failure, is one of the key factors for renal injury progression. Ectopic overexpression of Gal-3 significantly decreased the viability of HEK293, simultaneously inducing of cell cycle arrest and apoptosis. However, inhibition of Gal-3, mediated by modified citrus pectin (MCP), predominantly antagonized the pro-apoptotic effects. Mice were pre-treated with normal or 1% MCP-supplemented drinking water 1 week before cisplatin injection. Analyses of serum creatinine and renal tissue damage indicated that MCP-treated mice demonstrated increased renal function and attenuated renal fibrosis after cisplatin-induced injury. MCP-treated mice also demonstrated decreased renal fibrosis and apoptosis, as revealed by masson trichrome staining and Western blot analysis of cleaved caspase-3. Additionally, the protective role of Gal-3 inhibition in the kidney injury was shown to be mediated by protein kinase C α (PKC-α), which promoted cell apoptosis and collagen I synthesis in HEK293 cells. These results demonstrated the potential Gal-3 and PKC-α as therapeutic targets for the treatment of AKI and CKD.

Indexed as

Acute Kidney InjuryAnimalsApoptosisBlood ProteinsCaspase 3CisplatinCreatinineDisease Models, AnimalFibrosisGalectin 3GalectinsGene Expression RegulationHumansKidneyMiceNeoplasmsBlood ProteinsCaspase 3Cisplatincitrus pectinCreatinineGalectin 3GalectinsLGALS3 protein, humanPectinsProtein Kinase C-alphaacute kidney injuryapoptosisgalectin-3modified citrus pectinrenal fibrosis

Identifiers

PMID30455396
PMCPMC6435560
OpenAlexW2900934778

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Registered trials

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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.