Evidence map›Paper›PMID 31557402›Full record

ArticleJournal of cellular and molecular medicine2019

ALPK1 regulates streptozotocin-induced nephropathy through CCL2 and CCL5 expressions.

Chi-Pin Lee, Srinivasan Nithiyanantham, Hui-Ting Hsu, Kun-Tu Yeh, Tzer-Min Kuo, Ying-Chin Ko

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 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
4.6field-weighted citation impact, top 4% 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, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. The Role of Chemokines and Chemokine Receptors in Diabetic Nephropathy.International journal of molecular sciences · 2020
    Review
  14. Article
  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.

Chi-Pin LeeEnvironment-Omics-Disease Research Center, China Medical University Hospital, China Medical University, Taichung, Taiwan.
Srinivasan NithiyananthamEnvironment-Omics-Disease Research Center, China Medical University Hospital, China Medical University, Taichung, Taiwan.ORCID 0000-0001-9217-1269
Hui-Ting HsuDepartment of Surgical Pathology, Changhua Christian Hospital, Changhua, Taiwan.
Kun-Tu YehDepartment of Pathology, Changhua Christian Hospital, Changhua, Taiwan.
Tzer-Min KuoEnvironment-Omics-Disease Research Center, China Medical University Hospital, China Medical University, Taichung, Taiwan.
Ying-Chin KoEnvironment-Omics-Disease Research Center, China Medical University Hospital, China Medical University, Taichung, Taiwan.
China Medical University · TWChanghua Christian Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ALPK1 is associated with chronic kidney disease, gout and type 2 diabetes mellitus. Raised renal ALPK1 level in patients with diabetes was reported. Accelerated fibrotic nephropathies were observed in hyperglycaemic mice with up-regulated ALPK1. The aim of this study was to identify the mediators contributing to ALPK1 effect involving in nephropathies induction. The haematoxylin and eosin staining, Masson's trichrome and immunohistochemical analysis of ALPK1, NFkB, CCL2 and CCL5 were performed in the mice kidney. Cytokine antibody array analysis was performed in streptozotocin-treated wild-type mice (WT-STZ) and streptozotocin-treated ALPK1 transgenic mice (TG-STZ). The ALPK1 levels were measured in mice kidney and in cultured cells. We found that the higher levels of renal CCL2/MCP-1, CCL5/Rantes and G-CSF expression in TG-STZ compared with the WT-STZ. Glucose increased ALPK1 expressions in monocytic THP1 and human kidney-2 cells. The protein expression of ALPK1, NFkB and lectin was up-regulated in glucose-treated HK-2 cells. Knockdown of ALPK1 reduced CCL2 and CCL5 mRNA levels, whereas overexpressed ALPK1 increased CCL2 and CCL5 in cultured kidney cells. Taken together, these results show that high glucose increases ALPK1 and chemokine levels in the kidney. Elevated ALPK1 expression enhances renal CCL2 and CCL5 expressions in vivo and in vitro. ALPK1 is a mediator for CCL2 and CCL5 chemokine up-regulation involving in diabetic nephropathies induction.

Indexed as

AnimalsCell LineChemokine CCL2Chemokine CCL5ChemokinesGlucoseHumansKidneyKidney DiseasesMaleMice, Inbred C57BLMice, TransgenicNF-kappa BProtein KinasesRNA, MessengerStreptozocinALPK1 protein, humanChemokine CCL2Chemokine CCL5ChemokinesGlucoseNF-kappa BProtein KinasesRNA, MessengerStreptozocinALPK1CCL2CCL5chemokinediabetic nephropathy

Identifiers

PMID31557402
PMCPMC6815771
OpenAlexW2975107503

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.