Evidence map›Paper›PMID 25821833›Full record

ArticleJournal of diabetes research2015

Pituitary adenylate cyclase-activating polypeptide protects glomerular podocytes from inflammatory injuries.

Kenichi Sakamoto, Kyoko Kuno, Minoru Takemoto, Peng He, Takahiro Ishikawa, Shunichiro Onishi, Ryoichi Ishibashi, Emiko Okabe, Mayumi Shoji, Akiko Hattori and 6 more

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Network Pharmacology-Based Prediction of Mechanism of Shenzhuo Formula for Application to DKD.Evidence-based complementary and alternative medicine : eCAM · 2021
    Article
  4. Article
  5. Protective Effects of PACAP in Peripheral Organs.Frontiers in endocrinology · 2020
    Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. 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

16 authors at 2 institutions in 1 country.

Kenichi SakamotoDepartment of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, Chiba University Hospital, Japan.
Kyoko KunoDepartment of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Japan.
Minoru TakemotoDepartment of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, Chiba University Hospital, Japan.
Peng HeDepartment of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Japan.
Takahiro IshikawaDepartment of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, Chiba University Hospital, Japan.
Shunichiro OnishiDepartment of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, Chiba University Hospital, Japan.
Ryoichi IshibashiDepartment of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, Chiba University Hospital, Japan.
Emiko OkabeDepartment of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, Chiba University Hospital, Japan.
Mayumi ShojiDepartment of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, Chiba University Hospital, Japan.
Akiko HattoriDepartment of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, Chiba University Hospital, Japan.
Masaya YamagaDepartment of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, Chiba University Hospital, Japan.
Kazuki KobayashiDepartment of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, Chiba University Hospital, Japan.
Harukiyo KawamuraDepartment of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, Chiba University Hospital, Japan.
Hirotake TokuyamaDepartment of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, Chiba University Hospital, Japan.
Yoshiro MaezawaDepartment of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, Chiba University Hospital, Japan.
Koutaro YokoteDepartment of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, Chiba University Hospital, Japan.
Chiba University · JPChiba University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic nephropathy (DN) is a leading cause of end-stage kidney disease; however, there are few treatment options. Inflammation plays a crucial role in the initiation and/or progression of DN. Pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide, which was originally isolated from the ovine hypothalamus and reportedly has diverse biological functions. It has been reported that PACAP has renoprotective effects in different models of kidney pathology. However, the specific cell types within the kidney that are protected by PACAP have not yet been reported. In this study, we localized VPAC1, one of the PACAP receptors, to glomerular podocytes, which also reportedly has crucial roles not only in glomerular physiology but also in pathology. PACAP was effective in the downregulation of proinflammatory cytokines, such as monocyte chemoattractant protein-1 (MCP-1) and interleukin-6, which had been induced by the activation of toll-like receptor (TLR) with lipopolysaccharide. PACAP also had downregulated the expression of MCP-1 through the protein kinase A signaling pathway; this led to the attenuation of the activation of extracellular signal-regulated kinase and nuclear factor-kappa B signaling. Our results suggested that PACAP could be a possible treatment option for DN through the use of anti-inflammation effects on glomerular podocytes.

Indexed as

AnimalsAnti-Inflammatory AgentsChemokine CCL2Cyclic AMP-Dependent Protein KinasesDown-RegulationInflammationInterleukin-6KidneyKidney GlomerulusLipopolysaccharidesMaleMiceMice, Inbred C57BLNF-kappa BPituitary Adenylate Cyclase-Activating PolypeptidePodocytesAnti-Inflammatory AgentsChemokine CCL2Cyclic AMP-Dependent Protein KinasesInterleukin-6LipopolysaccharidesNF-kappa BPituitary Adenylate Cyclase-Activating PolypeptideTlr4 protein, mouseToll-Like Receptor 4Toll-Like Receptors

Identifiers

PMID25821833
PMCPMC4363873
OpenAlexW2105408302

What OpenQuestion holds

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LicenceCC BY
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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.