Evidence map›Paper›PMID 26728272›Full record

ArticleBMB reports2016

Neuropeptide Y protects kidney against cisplatin-induced nephrotoxicity by regulating p53-dependent apoptosis pathway.

Namoh Kim, Woo-Kie Min, Min Hee Park, Jong Kil Lee, Hee Kyung Jin, Jae-Sung Bae

Open access · goldAbstract readNews
In one paragraph

Article in BMB reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Neuropeptide Y Peptide Family and Cancer: Antitumor Therapeutic Strategies.International journal of molecular sciences · 2023
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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

6 authors at 1 institution in 1 country.

Namoh KimStem Cell Neuroplasticity Research Group, Kyungpook National University; Department of Physiology, Cell and Matrix Research Institute, School of Medicine, Kyungpook National University; Department of Biomedical Science, BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University, Daegu 41944, Korea.
Woo-Kie MinDepartment of Orthopaedic Surgery, Kyungpook National University Hospital, Daegu 41944, Korea.
Min Hee ParkStem Cell Neuroplasticity Research Group, Kyungpook National University; Department of Physiology, Cell and Matrix Research Institute, School of Medicine, Kyungpook National University; Department of Biomedical Science, BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University, Daegu 41944, Korea.
Jong Kil LeeStem Cell Neuroplasticity Research Group, Kyungpook National University; Department of Physiology, Cell and Matrix Research Institute, School of Medicine, Kyungpook National University; Department of Biomedical Science, BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University, Daegu 41944, Korea.
Hee Kyung JinStem Cell Neuroplasticity Research Group, Kyungpook National University; Department of Biomedical Science, BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University, Daegu 41944, Korea.
Jae-Sung BaeStem Cell Neuroplasticity Research Group, Kyungpook National University; Department of Physiology, Cell and Matrix Research Institute, School of Medicine, Kyungpook National University; Department of Biomedical Science, BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University, Daegu 41944, Korea.
Kyungpook National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cisplatin is a platinum-based chemotherapeutic drug for treating various types of cancers. However, the use of cisplatin is limited by its negative effect on normal tissues, particularly nephrotoxicity. Various mechanisms such as DNA adduct formation, mitochondrial dysfunction, oxidative stress, and apoptosis are involved in the adverse effect induced by cisplatin treatment. Several studies have suggested that neuropeptide Y (NPY) is involved in neuroprotection as well as restoration of bone marrow dysfunction from chemotherapy induced nerve injury. However, the role of NPY in chemotherapy- induced nephrotoxicity has not been studied. Here, we show that NPY rescues renal dysfunction by reducing the expression of pro-apoptotic proteins in cisplatin induced nephrotoxicity through Y1 receptor, suggesting that NPY can protect kidney against cisplatin nephrotoxicity as a possible useful agent to prevent and treat cisplatin-induced nephrotoxicity. [BMB Reports 2016; 49(5): 288-292].

Indexed as

AnimalsApoptosisCisplatinDown-RegulationFemaleKidneyKidney DiseasesMaleMice, Inbred C57BLNeuropeptide YProtective AgentsReceptors, Neuropeptide YSignal TransductionTumor Suppressor Protein p53CisplatinNeuropeptide Yneuropeptide Y-Y1 receptorProtective AgentsReceptors, Neuropeptide YTumor Suppressor Protein p53

Identifiers

PMID26728272
PMCPMC5070709
OpenAlexW2419177318

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.