Evidence map›Paper›PMID 26823720›Full record

ArticleInternational journal of clinical and experimental pathology2015

FK506 ameliorates podocyte injury in type 2 diabetic nephropathy by down-regulating TRPC6 and NFAT expression.

Ruixia Ma, Liqiu Liu, Wei Jiang, Yanjuan Yu, Haifeng Song

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Tacrolimus and diabetic rodent models.Pharmacological reports : PR · 2025
    Review
  2. A Putative Role for TRPC6 in Immune-Mediated Kidney Injury.International journal of molecular sciences · 2023
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Protective role of Trpc6 knockout in the progression of diabetic kidney disease.American journal of physiology. Renal physiology · 2018
    Article
  14. [Research advances in the association between transient receptor potential cation channel 6 and kidney disease].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2018
    Review
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

5 authors at 2 institutions in 1 country.

Ruixia MaDepartment of Nephrology, Affiliated Hospital of Qingdao University Qingdao, China.
Liqiu LiuDepartment of Nephrology, Affiliated Hospital of Qingdao University Qingdao, China.
Wei JiangDepartment of Nephrology, Affiliated Hospital of Qingdao University Qingdao, China.
Yanjuan YuDepartment of Special Medicine, Qingdao University Qingdao, China.
Haifeng SongDepartment of Urology, Peking University First Hospital Beijing, China.
Qingdao University · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic nephropathy (DN) is the leading cause of end-stage renal failure, and podocyte injury plays a major role in the development of DN. In this study, we investigated whether tacrolimus (FK506), an immunosuppressor, can attenuate podocyte injury in a type 2 diabetic mellitus (T2DM) rat model with DN. Transmission electron microcopy was used to morphologically evaluate renal injury. The urinary albumin (UAL), creatinine clearance rate (Ccr) and major biochemical parameters, including glucose, insulin, serum creatinine (Scr), urea nitrogen, total cholesterol (CHO) and triglyceride (TG), were examined 12 weeks after the administration of FK506. The expressions of the canonical transient receptor potential 6 (TRPC6), nuclear factor of activated T-cells (NFAT) and nephrin were detected by Western blotting and qPCR. In the rat model of DN, the expressions of TRPC6 and NFAT were significantly elevated compared with the normal rat group; however, the treatment with FK506 normalized the increased expression of TRPC6 and NFAT and attenuated podocyte ultrastructure injury. UAL, Ccr and the biochemical parameters were also improved by the use of FK506. In cell experiments, FK506 improved the decreased expression of nephrin and suppressed the elevated expression of both TRPC6 and NFAT caused by high glucose in accordance with TRPC6 blocker U73122. Our results demonstrated that FK506 could ameliorate podocyte injury in T2DM, which may be related to suppressed expressions of TRPC6 and NFAT.

Indexed as

AlbuminuriaAnimalsBiomarkersBlood GlucoseBlood Urea NitrogenCreatinineCytoprotectionDiabetes Mellitus, Type 2Diabetic NephropathiesDown-RegulationImmunosuppressive AgentsMaleMembrane ProteinsMicroscopy, Electron, TransmissionNFATC Transcription FactorsPodocytesBiomarkersBlood GlucoseCreatinineImmunosuppressive AgentsMembrane ProteinsnephrinNFATC Transcription FactorsTacrolimusTrpc6 protein, ratTRPC Cation ChannelsDiabetic nephropathyNFATpodocytetacrolimusTRPC6

Identifiers

PMID26823720
PMCPMC4713506
OpenAlexW2411553828

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.