Evidence map›Paper›PMID 27191747›Full record

ArticleOncotarget2016

CXCL16 regulates cisplatin-induced acute kidney injury.

Hua Liang, Zhengmao Zhang, Liqun He, Yanlin Wang

Abstract read
In one paragraph

Article in Oncotarget, 2016. 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
–field-weighted citation impact
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.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. The Role of CXCL16 in the Pathogenesis of Cancer and Other Diseases.International journal of molecular sciences · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. TAK1 deficiency attenuates cisplatin-induced acute kidney injury.American journal of physiology. Renal physiology · 2020
    Article
  17. Article
  18. Article
  19. Article
  20. CXCL16 is activated by p-JNK and is involved in HAmerican journal of translational research · 2018
    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

4 authors.

Hua LiangSelzman Institute for Kidney Health and Section of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas, United States of America.
Zhengmao ZhangSelzman Institute for Kidney Health and Section of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas, United States of America.
Liqun HeSection of Nephrology, Department of Medicine, Shuguang Hospital, Shanghai, China.
Yanlin WangSelzman Institute for Kidney Health and Section of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas, United States of America.

Funding

Cellular and Molecular Mechanisms of Renal FibrosisR01DK095835 · NIDDK · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI WANG, YANLIN · 2012 to 2021
$3.2M
Role of Bone Marrow-Derived Fibroblast Precursors in Cardiac FibrosisK08HL092958 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI WANG, YANLIN · 2009 to 2013
$655k
Targeting histone deacetylase 3 for chronic kidney diseaseI01BX002650 · VA · VA CONNECTICUT HEALTHCARE SYSTEM · PI YANLIN WANG · 2016 to 2026
–
BLRD VA I01 BX002650NHLBI NIH HHS K08 HL092958NIDDK NIH HHS R01 DK095835
6 · The paper itself

Abstract

The pathogenesis of cisplatin-induced acute kidney injury (AKI) is characterized by tubular cell apoptosis and inflammation. However, the molecular mechanisms are not fully understood. We found that CXCL16 was induced in renal tubular epithelial cells in response to cisplatin-induced AKI. Therefore, we investigated whether CXCL16 played a role in cisplatin-induced tubular cell apoptosis and inflammation. Wild-type and CXCL16 knockout mice were administrated with vehicle or cisplatin at 20 mg/kg by intraperitoneal injection. CXCL16 knockout mice had lower blood urea nitrogen and less tubular damage following cisplatin-induced AKI as compared with wild-type mice. Genetic disruption of CXCL16 reduced tubular epithelial cell apoptosis and decreased caspase-3 activation. Furthermore, CXCL16 deficiency inhibited infiltration of macrophages and T cells into the kidneys following cisplatin treatment, which was associated with reduced expression of the proinflammatory cytokines in the kidneys. Taken together, our results indicate that CXCL16 plays a crucial role in the pathogenesis of cisplatin-induced AKI through regulation of apoptosis and inflammation and maybe a novel therapeutic target for cisplatin-induced AKI.

Indexed as

ApoptosisCisplatinAcute Kidney InjuryAnimalsCaspase 3Chemokine CXCL16Chemotaxis, LeukocyteDisease Models, AnimalGenetic Predisposition to DiseaseInflammation MediatorsKidneyMacrophagesMaleMice, Inbred C57BLMice, KnockoutNephritisCasp3 protein, mouseCaspase 3Chemokine CXCL16CisplatinCxcl16 protein, mouseInflammation Mediatorsacute kidney injuryapoptosischemokinescisplatincytokines

Identifiers

PMID27191747
PMCPMC5077966

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.