Evidence map›Paper›PMID 26498843›Full record

ArticleBMC nephrology2015

Intermedin protects against renal ischemia-reperfusion injury by inhibiting endoplasmic reticulum stress.

Yanhong Wang, Jihua Tian, Xi Qiao, Xiaole Su, Yang Mi, Ruijing Zhang, Rongshan Li

Open access · goldAbstract read
In one paragraph

Article in BMC nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  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 1 country.

Yanhong WangDepartment of Microbiology and Immunology, Shanxi Medical University, Taiyuan, Shanxi, China. wangyanhongmail@126.com.
Jihua TianDepartment of Microbiology and Immunology, Shanxi Medical University, Taiyuan, Shanxi, China. jihutian429@163.com.
Xi QiaoDepartment of Nephrology, Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, China. qiaoxi7347@163.com.
Xiaole SuDepartment of Nephrology, Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, China. kunle6609@163.com.
Yang MiDepartment of Microbiology and Immunology, Shanxi Medical University, Taiyuan, Shanxi, China. 285055160@qq.com.
Ruijing ZhangDepartment of Nephrology, Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, China. zhangruijing_0105@163.com.
Rongshan LiDepartment of Nephrology, the Affiliated People's Hospital of Shanxi Medical University, Shanxi Provincial People's Hospital, Shanxi Kidney Disease Institute, No. 29 Shuang Ta East Street, Taiyuan, 030012, , Shanxi, P. R. China. rongshanli13@163.com.
Shanxi Medical University · CNSecond Hospital of Shanxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIntermedin (IMD) is a novel member of the calcitonin/calcitonin gene-related peptide family. Endoplasmic reticulum stress (ERS) has been implicated in the pathology of renal ischemia/reperfusion (IRI). In the present study, we investigated whether IMD could reduce ERS damage after renal ischemia.

methodsThe kidneys of SD rats were subjected to 45 min of warm ischemia followed by 24 h of reperfusion. The hypoxia/reoxygenation(H/R) model in NRK-52E cells consisted of hypoxia for 1 h and reoxygenation for 2 h. IMD was over-expressed in vivo and in vitro using the vector pcDNA3.1-IMD. The serum creatinine concentration and lactate dehydrogenase (LDH) activity in the plasma were determined. Histologic examinations of renal tissues were performed with PAS staining. Real-time PCR and Western blotting were used to determine the mRNA and protein levels, respectively. Additionally, ER staining was used to detect the ERS response.

resultsIn the rat renal IRI model, we found that IMD gene transfer markedly improved renal function and pathology and decreased LDH activity and cell apoptosis compared with the kidneys that were transfected with the control plasmid. IMD significantly attenuated the ERS stress parameters compared with IRI group. Indeed, IMD down-regulated glucose-regulated protein 78 (GRP78), C/EBP homologous protein(CHOP), and caspase 12 protein and mRNA levels. Moreover, in the NRK-52E cell H/R model, IMD overexpression prevented the apoptosis induced by H/R. Furthermore, IMD ameliorated the ER structural changes and concomitantly decreased the levels of GRP78, CHOP and caspase-12.

conclusionThis study revealed that IMD protects against renal IRI by suppressing ERS and ERS-related apoptosis.

Indexed as

Endoplasmic Reticulum StressAdrenomedullinAnimalsApoptosisCaspase 12Cell LineCreatinineEndoplasmic Reticulum Chaperone BiPEpithelial CellsGene ExpressionHeat-Shock ProteinsHydro-LyasesKidney TubulesMaleNeuropeptidesRatsAdm2 protein, ratAdrenomedullinCaspase 12CreatinineDdit3 protein, ratEndoplasmic Reticulum Chaperone BiPGRP78 protein, ratHeat-Shock ProteinsHydro-Lyaseslactate dehydrataseNeuropeptidesTranscription Factor CHOP

Identifiers

PMID26498843
PMCPMC4619099
OpenAlexW2142461695

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.