Evidence map›Paper›PMID 31101909›Full record

ArticleScientific reports2019

Dipeptidyl peptidase-4 plays a pathogenic role in BSA-induced kidney injury in diabetic mice.

Yuta Takagaki, Sen Shi, Makoto Katoh, Munehiro Kitada, Keizo Kanasaki, Daisuke Koya

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. The Role of PKM2 in Diabetic Microangiopathy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022
    Review
  9. Therapy of Type 2 Diabetes in Patients with SARS-CoV-2 Infection.International journal of molecular sciences · 2021
    Review
  10. Article
  11. Article
  12. Renoprotective Effects of DPP-4 Inhibitors.Antioxidants (Basel, Switzerland) · 2021
    Review
  13. DPP4 Inhibitors and COVID-19-Holy Grail or Another Dead End?Archivum immunologiae et therapiae experimentalis · 2021
    Review
  14. Review
  15. 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

6 authors at 2 institutions in 1 country.

Yuta TakagakiDepartment of Diabetology and Endocrinology, Kanazawa Medical University, Uchinada, Ishikawa, 920-0293, Japan.
Sen ShiDepartment of Diabetology and Endocrinology, Kanazawa Medical University, Uchinada, Ishikawa, 920-0293, Japan.
Makoto KatohMitsubishi Tanabe Pharma Corporation Ikuyaku, Integrated Value Development Division, Tokyo, Japan.
Munehiro KitadaDepartment of Diabetology and Endocrinology, Kanazawa Medical University, Uchinada, Ishikawa, 920-0293, Japan.
Keizo KanasakiDepartment of Diabetology and Endocrinology, Kanazawa Medical University, Uchinada, Ishikawa, 920-0293, Japan. kkanasak@kanazawa-med.ac.jp.ORCID http://orcid.org/0000-0002-9563-502X
Daisuke KoyaDepartment of Diabetology and Endocrinology, Kanazawa Medical University, Uchinada, Ishikawa, 920-0293, Japan. koya0516@kanazawa-med.ac.jp.
Kanazawa Medical University · JPMitsubishi Group (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic kidney disease (DKD) is appeared to be higher risk of declining kidney function compared to non-diabetic kidney disease with same magnitude of albuminuria. Epithelial-mesenchymal transition (EMT) program of tubular epithelial cells (TECs) could be important for the production of the extracellular matrix in the kidney. Caveolin-1 (CAV1), dipeptidyl peptidase-4 (DPP-4) and integrin β1 have shown to be involved in EMT program. Here, we found diabetic kidney is prone for albuminuria-induced TECs damage and DPP-4 plays a vital role in such parenchymal damages in diabetic mice. The bovine serum albumin (BSA) injection induced severe TECs damage and altered expression levels of DPP-4, integrin β1, CAV1, and EMT programs including relevant microRNAs in type 1 diabetic CD-1 mice when compared to non-diabetic mice; teneligliptin (TENE) ameliorated these alterations. TENE suppressed the close proximity among DPP-4, integrin β1 and CAV1 in a culture of HK-2 cells. These findings suggest that DPP-4 inhibition can be relevant for combating proteinuric DKD by targeting the EMT program induced by the crosstalk among DPP-4, integrin β1 and CAV1.

Indexed as

AnimalsCaveolin 1Diabetes Mellitus, ExperimentalDiabetic NephropathiesDipeptidyl Peptidase 4Dipeptidyl-Peptidase IV InhibitorsEpithelial-Mesenchymal TransitionFibrosisHumansIntegrin beta1Kidney TubulesMaleMicePyrazolesSerum Albumin, BovineSignal Transduction3-(4-(4-(3-methyl-1-phenyl-1H-pyrazol-5-yl)piperazin-1-yl)pyrrolidin-2-ylcarbonyl)thiazolidineCav1 protein, mouseCaveolin 1Dipeptidyl Peptidase 4Dipeptidyl-Peptidase IV InhibitorsDpp4 protein, mouseIntegrin beta1PyrazolesSerum Albumin, BovineSmad3 ProteinSmad3 protein, mouseThiazolidinesTransforming Growth Factor beta

Identifiers

PMID31101909
PMCPMC6525172
OpenAlexW2945862141

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.