Evidence map›Paper›PMID 27580845›Full record

ArticleScientific reports2016

Calcineurin inhibitors cyclosporin A and tacrolimus protect against podocyte injury induced by puromycin aminonucleoside in rodent models.

Xiujin Shen, Hong Jiang, Meike Ying, Zhoutao Xie, Xiayu Li, Haibing Wang, Jie Zhao, Chuan Lin, Yucheng Wang, Shi Feng and 13 more

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 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
4.1field-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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Pooled it
  2. WNK1 Kinase Activity Is Required for the Functional Maintenance of Podocyte Structure.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
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  4. Sexual Dimorphism in Renal Progenitors: Do Immunosuppressants Erase the Female Advantage?Transplant international : official journal of the European Society for Organ Transplantation · 2026
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. The CaPediatric nephrology (Berlin, Germany) · 2025
    Review
  10. Acute kidney injury in paediatric kidney transplant recipients.Pediatric nephrology (Berlin, Germany) · 2025
    Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
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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

23 authors at 7 institutions in 2 countries.

Xiujin ShenKidney Disease Center, First Affiliated Hospital, Zhejiang University, School of Medicine; Key Laboratory of Nephropathy, Zhejiang Province, Hangzhou, Zhejiang, China.
Hong JiangKidney Disease Center, First Affiliated Hospital, Zhejiang University, School of Medicine; Key Laboratory of Nephropathy, Zhejiang Province, Hangzhou, Zhejiang, China.
Meike YingKidney Disease Center, First Affiliated Hospital, Zhejiang University, School of Medicine; Key Laboratory of Nephropathy, Zhejiang Province, Hangzhou, Zhejiang, China.
Zhoutao XieKidney Disease Center, First Affiliated Hospital, Zhejiang University, School of Medicine; Key Laboratory of Nephropathy, Zhejiang Province, Hangzhou, Zhejiang, China.
Xiayu LiKidney Disease Center, First Affiliated Hospital, Zhejiang University, School of Medicine; Key Laboratory of Nephropathy, Zhejiang Province, Hangzhou, Zhejiang, China.
Haibing WangNational Clinical Research Base of Traditional Chinese Medicine, Zhejiang Hospital of Traditional Chinese Medicine, Zhejiang Chinese Medical University, Hangzhou, China.
Jie ZhaoKidney Disease Center, First Affiliated Hospital, Zhejiang University, School of Medicine; Key Laboratory of Nephropathy, Zhejiang Province, Hangzhou, Zhejiang, China.
Chuan LinKidney Disease Center, First Affiliated Hospital, Zhejiang University, School of Medicine; Key Laboratory of Nephropathy, Zhejiang Province, Hangzhou, Zhejiang, China.
Yucheng WangKidney Disease Center, First Affiliated Hospital, Zhejiang University, School of Medicine; Key Laboratory of Nephropathy, Zhejiang Province, Hangzhou, Zhejiang, China.
Shi FengKidney Disease Center, First Affiliated Hospital, Zhejiang University, School of Medicine; Key Laboratory of Nephropathy, Zhejiang Province, Hangzhou, Zhejiang, China.
Jia ShenKidney Disease Center, First Affiliated Hospital, Zhejiang University, School of Medicine; Key Laboratory of Nephropathy, Zhejiang Province, Hangzhou, Zhejiang, China.
Chunhua WengKidney Disease Center, First Affiliated Hospital, Zhejiang University, School of Medicine; Key Laboratory of Nephropathy, Zhejiang Province, Hangzhou, Zhejiang, China.
Weiqiang LinKidney Disease Center, First Affiliated Hospital, Zhejiang University, School of Medicine; Key Laboratory of Nephropathy, Zhejiang Province, Hangzhou, Zhejiang, China.
Huiping WangKidney Disease Center, First Affiliated Hospital, Zhejiang University, School of Medicine; Key Laboratory of Nephropathy, Zhejiang Province, Hangzhou, Zhejiang, China.
Qin ZhouKidney Disease Center, First Affiliated Hospital, Zhejiang University, School of Medicine; Key Laboratory of Nephropathy, Zhejiang Province, Hangzhou, Zhejiang, China.
Yan BiKidney Disease Center, First Affiliated Hospital, Zhejiang University, School of Medicine; Key Laboratory of Nephropathy, Zhejiang Province, Hangzhou, Zhejiang, China.
Meng LiKidney Disease Center, First Affiliated Hospital, Zhejiang University, School of Medicine; Key Laboratory of Nephropathy, Zhejiang Province, Hangzhou, Zhejiang, China.
Lingyan WangBiomedical Research Center, Zhongshan Hospital, Fudan University, Shanghai, China.
Tongyu ZhuDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai, China.
Xiaoru HuangLi Ka Shing Institute of Health Sciences, and Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong, China.
Hui-Yao LanLi Ka Shing Institute of Health Sciences, and Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong, China.
Jing ZhouHarvard Center for Polycystic Kidney Disease Research and Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, USA.
Jianghua ChenKidney Disease Center, First Affiliated Hospital, Zhejiang University, School of Medicine; Key Laboratory of Nephropathy, Zhejiang Province, Hangzhou, Zhejiang, China.
First Affiliated Hospital Zhejiang University · CNArkana Laboratories · USChinese University of Hong Kong · CNZhejiang Chinese Medical University · CNBrigham and Women's Hospital · USThe First Affiliated Hospital, Sun Yat-sen University · CNZhongshan Hospital · CN

Funding

Cell biology of autosomal dominant polycystic kidney diseaseR01DK099532 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI ZHOU, JING · 2014 to 2016
$796k
NIDDK NIH HHS R01 DK099532
6 · The paper itself

Abstract

Podocyte injury and the appearance of proteinuria are features of minimal-change disease (MCD). Cyclosporin A (CsA) and tacrolimus (FK506) has been reported to reduce proteinuria in patients with nephrotic syndrome, but mechanisms remain unknown. We, therefore, investigated the protective mechanisms of CsA and FK506 on proteinuria in a rat model of MCD induced by puromycin aminonucleoside (PAN) and in vitro cultured mouse podocytes. Our results showed that CsA and FK506 treatment decreased proteinuria via a mechanism associated to a reduction in the foot-process fusion and desmin, and a recovery of synaptopodin and podocin. In PAN-treated mouse podocytes, pre-incubation with CsA and FK506 restored the distribution of the actin cytoskeleton, increased the expression of synaptopodin and podocin, improved podocyte viability, and reduced the migrating activities of podocytes. Treatment with CsA and FK506 also inhibited PAN-induced podocytes apoptosis, which was associated with the induction of Bcl-xL and inhibition of Bax, cleaved caspase 3, and cleaved PARP expression. Further studies revealed that CsA and FK506 inhibited PAN-induced p38 and JNK signaling, thereby protecting podocytes from PAN-induced injury. In conclusion, CsA and FK506 inhibit proteinuria by protecting against PAN-induced podocyte injury, which may be associated with inhibition of the MAPK signaling pathway.

Indexed as

Calcineurin InhibitorsAnimalsApoptosisCell LineCyclosporineMaleMAP Kinase Signaling SystemMiceNephrosis, LipoidPodocytesProteinuriaPuromycin AminonucleosideRats, Sprague-DawleyTacrolimusCalcineurin InhibitorsCyclosporinePuromycin AminonucleosideTacrolimus

Identifiers

PMID27580845
PMCPMC5007516
OpenAlexW2517089249

What OpenQuestion holds

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LicenceCC BY
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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.