Evidence map›Paper›PMID 25898836›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2015

Autophagy activation attenuates renal ischemia-reperfusion injury in rats.

Ya-Li Zhang, Jie Zhang, Li-Yan Cui, Shuo Yang

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

35 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
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  8. Review
  9. Review
  10. Article
  11. Roles of NADInternational journal of molecular sciences · 2022
    Review
  12. Article
  13. Article
  14. Autophagy and Renal Fibrosis.Aging and disease · 2022
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. 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

4 authors at 2 institutions in 1 country.

Ya-Li ZhangDepartment of Laboratory Medicine, Peking University Third Hospital, Beijing 100191, China.
Jie ZhangDepartment of Laboratory Medicine, Peking University Third Hospital, Beijing 100191, China bjmuzhangjie@sina.com.
Li-Yan CuiDepartment of Laboratory Medicine, Peking University Third Hospital, Beijing 100191, China.
Shuo YangDepartment of Laboratory Medicine, Peking University Third Hospital, Beijing 100191, China.
Peking University · CNPeking University Third Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemia-reperfusion (I/R) injury is a leading cause of acute kidney injury (AKI), which is a common clinical complication but lacks effective therapies. This study investigated the role of autophagy in renal I/R injury and explored potential mechanisms in an established rat renal I/R injury model. Forty male Wistar rats were randomly divided into four groups: Sham, I/R, I/R pretreated with 3-methyladenine (3-MA, autophagy inhibitor), or I/R pretreated with rapamycin (autophagy activator). All rats were subjected to clamping of the left renal pedicle for 45 min after right nephrectomy, followed by 24 h of reperfusion. The Sham group underwent the surgical procedure without ischemia. 3-MA and rapamycin were injected 15 min before ischemia. Renal function was indicated by blood urea nitrogen and serum creatinine. Tissue samples from the kidneys were scored histopathologically. Autophagy was indicated by light chain 3 (LC3), Beclin-1, and p62 levels and the number of autophagic vacuoles. Apoptosis was evaluated by the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) method and expression of caspase-3. Autophagy was activated after renal I/R injury. Inhibition of autophagy by 3-MA before I/R aggravated renal injury, with worsened renal function, higher renal tissue injury scores, and more tubular apoptosis. In contrast, rapamycin pretreatment ameliorated renal injury, with improved renal function, lower renal tissue injury scores, and inhibited apoptosis based on fewer TUNEL-positive cells and lower caspase-3 expression. Our results demonstrate that autophagy could be activated during I/R injury and play a protective role in renal I/R injury. The mechanisms were involved in the regulation of several autophagy and apoptosis-related genes. Furthermore, autophagy activator may be a promising therapy for I/R injury and AKI in the future.

Indexed as

Acute Kidney InjuryAdenineAnimalsApoptosisAutophagyBlood Urea NitrogenCaspase 3CreatinineDisease Models, AnimalIn Situ Nick-End LabelingMaleRatsRats, WistarReperfusion InjurySirolimus3-methyladenineAdenineCaspase 3CreatinineSirolimusacute kidney injuryapoptosisAutophagyischemia reperfusion

Identifiers

PMID25898836
PMCPMC4935330
OpenAlexW1997930185

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.