Evidence map›Paper›PMID 28425936›Full record

ArticleNutrients2017

Genistein Ameliorates Ischemia/Reperfusion-Induced Renal Injury in a SIRT1-Dependent Manner.

Wei-Fang Li, Kang Yang, Ping Zhu, Hong-Qian Zhao, Yin-Hong Song, Kuan-Can Liu, Wei-Feng Huang

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. NADCell communication and signaling : CCS · 2024
    Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Journal of traditional and complementary medicine · 2022
    Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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.

Wei-Fang LiMedical College, China Three Gorges University, Yichang 443002, China. lwf199023@163.com.
Kang YangMedical College, China Three Gorges University, Yichang 443002, China. yangkang0218@126.com.
Ping ZhuDepartment of Medicine, the First College of Clinical Medical Science, China Three Gorges University, Yichang 443002, China. topgan2000@163.com.
Hong-Qian ZhaoMedical College, China Three Gorges University, Yichang 443002, China. 15271506793@163.com.
Yin-Hong SongMedical College, China Three Gorges University, Yichang 443002, China. syh728@126.com.
Kuan-Can LiuInstitute for Laboratory Medicine, Fuzhou General Hospital, PLA, Fuzhou 350025, China. liukuancan@163.com.
Wei-Feng HuangMedical College, China Three Gorges University, Yichang 443002, China. huangweifeng@ctgu.edu.cn.
China Three Gorges University · CNColumbia University Irving Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal ischemia/reperfusion (I/R) injury continues to be a complicated situation in clinical practice. Genistein, the main isoflavone found in soy products, is known to possess a wide spectrum of biochemical and pharmacological activities. However, the protective effect of genistein on renal I/R injury has not been well investigated. In the current study, we explore whether genistein exhibits its renal-protective effects through SIRT1 (Sirtuin 1) in I/R-induced mice model. We found the treatment of genistein significantly reduced renal I/R-induced cell death, simultaneously stimulating renal cell proliferation. Meanwhile, SIRT1 expression was up-regulated following the administration of genistein in renal region. Furthermore, pharmacological inhibition or shRNA-mediated depletion of SIRT1 significantly reversed the protective effect of genistein on renal dysfunction, cellular damage, apoptosis, and proliferation following I/R injury, suggesting an indispensible role of the increased SIRT1 expression and activity in this process. Meanwhile, the reduced p53 and p21 expression and increased PCNA (Proliferating Cell Nuclear Antigen) expression were blocked after the depletion of SIRT1 compared with the genistein treatment group in the renal I/R process. Hence, our results provided further experimental basis for the potential use of genistein for the treatment of kidney disease with deficiency of SIRT1 activity.

Indexed as

AnimalsApoptosisCell ProliferationCyclin-Dependent Kinase Inhibitor p21Disease Models, AnimalGenisteinKidneyKidney DiseasesMiceMice, Inbred BALB CProliferating Cell Nuclear AntigenReperfusion InjurySirtuin 1Tumor Suppressor Protein p53Cdkn1a protein, mouseCyclin-Dependent Kinase Inhibitor p21GenisteinProliferating Cell Nuclear AntigenSirt1 protein, mouseSirtuin 1Tumor Suppressor Protein p53genisteinrenal ischemia-reperfusionSIRT1

Identifiers

PMID28425936
PMCPMC5409742
OpenAlexW2606491448

What OpenQuestion 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 OpenQuestion graph.