Evidence map›Paper›PMID 16400005›Full record

ArticleThe American journal of pathology2006

Growth factor midkine is involved in the pathogenesis of diabetic nephropathy.

Tomoki Kosugi, Yukio Yuzawa, Waichi Sato, Hanayo Kawai, Seiichi Matsuo, Yoshifumi Takei, Takashi Muramatsu, Kenji Kadomatsu

Open access · hybridAbstract read
In one paragraph

Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.8field-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

26 citing papers in PubMed, 58 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Midkine-A novel player in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022
    Review
  7. Article
  8. Observational
  9. Observational
  10. Midkine in vitamin D deficiency and its association with anti-Saccharomyces cerevisiae antibodies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Midkine in inflammation.TheScientificWorldJournal · 2011
    Review
  18. Review
  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

8 authors at 2 institutions in 1 country.

Tomoki KosugiDepartment of Biochemistry, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan.
Yukio Yuzawa
Waichi Sato
Hanayo Kawai
Seiichi Matsuo
Yoshifumi Takei
Takashi Muramatsu
Kenji Kadomatsu
Nagoya University · JPAichi Gakuin University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic nephropathy is a life-threatening disease associated with diabetes mellitus. Longstanding hyperglycemia induces pathological reactions of glomerular mesangial cells, such as overproduction of extracellular matrix, which finally lead to nephropathy. However, the mechanisms underlying its pathogenesis have not been completely elucidated. Using the Streptozotocin-induced model of diabetes, we report that mice deficient in the growth factor midkine (Mdk-/-) exhibited strikingly milder nephropathy than Mdk+/+ mice, even though both mice showed similar extents of hyperglycemia after Streptozotocin injection. Midkine expression was induced in the glomerular mesangium of Mdk+/+ mice with diabetic nephropathy and in primary cultured mesangial cells exposed to high glucose. Mdk-/- mesangial cells exhibited reduced phosphorylation of protein kinase C and extracellular signal-regulated kinase as well as reduced production of transforming growth factor-beta(1) on high glucose loading. Addition of exogenous midkine restored extracellular signal-regulated kinase phosphorylation in Mdk-/- cells under high glucose conditions, whereas a midkine antisense oligodeoxynucleotide suppressed midkine in Mdk+/+ cells. Therefore, this study identifies midkine as a key molecule in diabetic nephropathy and suggests that midkine accelerates the intracellular signaling network evoked by hyperglycemia in nephropathy.

Indexed as

AnimalsBlotting, WesternCells, CulturedCytokinesDiabetes Mellitus, ExperimentalDiabetic NephropathiesEnzyme-Linked Immunosorbent AssayExtracellular Signal-Regulated MAP KinasesFemaleGlomerular MesangiumHyperglycemiaImmunohistochemistryMiceMice, Mutant StrainsMidkineProtein Kinase CCytokinesExtracellular Signal-Regulated MAP KinasesMidkineProtein Kinase CTgfb1 protein, mouseTransforming Growth Factor betaTransforming Growth Factor beta1

Identifiers

PMID16400005
PMCPMC1592654
OpenAlexW2027274931

What OpenQuestion holds

Textmetadata
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.