Evidence map›Paper›PMID 29600538›Full record

ArticleJournal of cellular biochemistry2018

SB-216763, a GSK-3β inhibitor, protects against aldosterone-induced cardiac, and renal injury by activating autophagy.

Yi-De Zhang, Xiao-Jun Ding, Hou-Yong Dai, Wei-Sheng Peng, Nai-Feng Guo, Yuan Zhang, Qiao-Ling Zhou, Xiao-Lan Chen

Open access · hybridAbstract read
In one paragraph

Article in Journal of cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
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  13. Review
  14. Targeting the Wnt Signaling Pathway in Liver Fibrosis for Drug Options: An Update.Journal of clinical and translational hepatology · 2021
    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

8 authors at 2 institutions in 1 country.

Yi-De ZhangDepartment of Nephrology, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Xiao-Jun DingDepartment of Cardiology, Affiliated Danyang People's Hospital of Nantong University, Danyang, China.
Hou-Yong DaiDepartment of Nephrology, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Wei-Sheng PengDepartment of Nephrology, Affiliated Xiangya Hospital of Central South University, Changsha, Hunan, China.
Nai-Feng GuoDepartment of Nephrology, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Yuan ZhangDepartment of Nephrology, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Qiao-Ling ZhouDepartment of Nephrology, Affiliated Xiangya Hospital of Central South University, Changsha, Hunan, China.
Xiao-Lan ChenDepartment of Nephrology, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.ORCID 0000-0003-0732-713X
Nantong University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular and renal inflammation induced by Aldosterone (Aldo) plays a pivotal role in the pathogenesis of hypertension and renal fibrosis. GSK-3β contributes to inflammatory cardiovascular and renal diseases, but its role in Aldo-induced hypertension, and renal damage is not clear. In the present study, rats were treated with Aldo combined with SB-216763 (a GSK-3β inhibitor) for 4 weeks. Hemodynamic, cardiac, and renal parameters were assayed at the indicated time. Here we found that rats treated with Aldo presented cardiac and renal hypertrophy and dysfunction. Cardiac and renal expression levels of molecular markers attesting inflammation and fibrosis were increased by Aldo infusion, whereas the treatment of SB-216763 reversed these alterations. SB-216763 suppressed cardiac and renal inflammatory cytokines levels (TNF-a, IL-1β, and MCP-1). Meanwhile, SB-216763 increased the protein levels of LC3-II in the cardiorenal tissues as well as p62 degradation, indicating that SB-216763 induced autophagy activation in cardiac, and renal tissues. Importantly, inhibition of autophagy by 3-MA attenuated the role of SB-216763 in inhibiting perivascular fibrosis, and tubulointerstitial injury. These data suggest that SB-216763 protected against Aldo-induced cardiac and renal injury by activating autophagy, and might be a therapeutic option for salt-sensitive hypertension and renal fibrosis.

Indexed as

AutophagyAldosteroneAnimalsCytokinesFibrosisGlycogen Synthase Kinase 3 betaHeart DiseasesIndolesInflammationKidney DiseasesMaleMaleimidesRatsRats, WistarAldosteroneCytokinesGlycogen Synthase Kinase 3 betaIndolesMaleimidesSB 216763aldosteroneautophagycardiac and renal injuryGSK-3β inhibitor

Identifiers

PMID29600538
PMCPMC6001754
OpenAlexW2795041628

What OpenQuestion holds

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LicenceCC BY
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.