Evidence map›Paper›PMID 27857162›Full record

ArticleScientific reports2016

Rescue therapy with Tanshinone IIA hinders transition of acute kidney injury to chronic kidney disease via targeting GSK3β.

Chunming Jiang, Wei Zhu, Xiang Yan, Qiuyuan Shao, Biao Xu, Miao Zhang, Rujun Gong

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
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  16. Interleukin-10 attenuates renal injury after myocardial infarction in diabetes.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2022
    Article
  17. Folic acid-induced animal model of kidney disease.Animal models and experimental medicine · 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

7 authors at 2 institutions in 2 countries.

Chunming JiangDepartment of Nephrology, Affiliated Nanjing Drum Tower Hospital, Nanjing University School of Medicine, Nanjing, China.
Wei ZhuDepartment of Nephrology, Affiliated Nanjing Drum Tower Hospital, Nanjing University School of Medicine, Nanjing, China.
Xiang YanDepartment of Urology, Affiliated Nanjing Drum Tower Hospital, Nanjing University School of Medicine, Nanjing, China.
Qiuyuan ShaoDepartment of Nephrology, Affiliated Nanjing Drum Tower Hospital, Nanjing University School of Medicine, Nanjing, China.
Biao XuDepartment of Cardiology, Affiliated Nanjing Drum Tower Hospital, Nanjing University School of Medicine, Nanjing, China.
Miao ZhangDepartment of Nephrology, Affiliated Nanjing Drum Tower Hospital, Nanjing University School of Medicine, Nanjing, China.
Rujun GongDivision of Kidney Disease and Hypertension, Department of Medicine, Rhode Island Hospital, Brown University School of Medicine, Providence, Rhode Island, USA.
Nanjing Drum Tower Hospital · CNBrown University · US

Funding

Therapeutic targeting of GSK3beta: A novel approach for podocyte protectionR01DK092485 · NIDDK · RHODE ISLAND HOSPITAL · PI GONG, RUJUN · 2011 to 2015
$1.8M
NIDDK NIH HHS R01 DK092485
6 · The paper itself

Abstract

Acute kidney injury (AKI) remains challenging for clinical practice and poses a risk of developing progressive chronic kidney disease (CKD) with no definitive treatment available yet. Tanshinone IIA, an active ingredient of Chinese herbal Salvia miltiorrhiza, has been widely used in Asia for the remarkable organoprotective activities. Its effect on established AKI, however, remains unknown. In mice with folic acid-induced AKI, delayed treatment with Tanshinone IIA, commenced early or late after injury, diminished renal expression of kidney injury markers, reduced apoptosis and improved kidney dysfunction, concomitant with mitigated histologic signs of AKI to CKD transition, including interstitial fibrosis and tubular atrophy, and with an ameliorated inflammatory infiltration in tubulointerstitium and a favored M2-skewed macrophage polarization. Mechanistically, Tanshinone IIA blunted glycogen synthase kinase (GSK)3β overactivity and hyperactivation of its downstream mitogen-activated protein kinases that are centrally implicated in renal fibrogenesis and inflammation. Inhibition of GSK3β is likely a key mechanism mediating the therapeutic activity of Tanshinone IIA, because sodium nitroprusside, a GSK3β activator, largely offset its renoprotective effect. In confirmatory studies, rescue treatment with Tanshinone IIA likewise ameliorated ischemia/reperfusion-induced kidney destruction in mice. Our data suggest that Tanshinone IIA represents a valuable treatment that improves post-AKI kidney salvage via targeting GSK3β.

Indexed as

AbietanesAcute Kidney InjuryAnimalsFolic AcidGlycogen Synthase Kinase 3 betaKidneyKidney Failure, ChronicKidney Function TestsMacrophagesMAP Kinase Signaling SystemMiceAbietanesFolic AcidGlycogen Synthase Kinase 3 betatanshinone

Identifiers

PMID27857162
PMCPMC5114614
OpenAlexW2554604774

What Socratic holds

Textmetadata
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 Socratic graph.