Evidence map›Paper›PMID 32632610›Full record

Trial reportMolecular and cellular biochemistry2020

Leptin promotes endothelial dysfunction in chronic kidney disease by modulating the MTA1-mediated WNT/β-catenin pathway.

Bing Liu, Jiao Qiao, Jinxiu Hu, Minghua Fan, Yanfang Zhao, Hong Su, Ziyang Wang, Qun Yu, Qiqi Ma, Yanmei Li and 2 more

Abstract readClinical Trial
PubMed Publisher
In one paragraph

Trial report in Molecular and cellular biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Childhood Obesity: Insight into Kidney Involvement.International journal of molecular sciences · 2023
    Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Adipokines and Inflammation: Focus on Cardiovascular Diseases.International journal of molecular sciences · 2020
    Review
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

12 authors at 3 institutions in 1 country.

Bing LiuDepartment of Nephrology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China.
Jiao QiaoDepartment of Nephrology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China.
Jinxiu HuDepartment of Nephrology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China.
Minghua FanDepartment of Obstetrics and Gynecology, The Second Hospital of Shandong University, Jinan, 250021, Shandong, China.
Yanfang ZhaoDepartment of Nephrology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China.
Hong SuDepartment of Nephrology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China.
Ziyang WangDepartment of Nephrology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China.
Qun YuDepartment of Nephrology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China.
Qiqi MaShandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, China.
Yanmei LiDepartment of Nephrology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China.
Zhimei LvDepartment of Nephrology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China. sdlvzhimei@163.com.ORCID http://orcid.org/0000-0003-1634-883X
Rong WangDepartment of Nephrology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China. Wangrong_sd@126.com.
Shandong University · CNSecond Hospital of Shandong University · CNShandong Provincial Hospital · CN

Funding

National Natural Science Foundation of China 81370834National Natural Science Foundation of China 81400732National Natural Science Foundation of China 81770723National Natural Science Foundation of China 81873615Taishan Scholars Program of Shandong Province ts201712090Taishan Scholars Program of Shandong Province tsqn201812138The Science and Technology Innovation Program of Clinical Medicine from the Jinan Science and Technology Bureau 201805001The Science and Technology Innovation Program of Clinical Medicine from the Jinan Science and Technology Bureau 201805054
6 · The paper itself

Abstract

Endothelial dysfunction (ED) has a high incidence in chronic kidney disease (CKD) and is identified as a precursor to cardiovascular events. Recent studies suggest that leptin may be the missing link between ED and CKD. The objective of this study was to investigate the mechanism by which leptin causes ED and the connection with leptin and indicators of ED in CKD patients. Analysis of leptin-treated human umbilical vein endothelial cells (HUVECs) showed increased expression of interleukin 6 (IL-6), endothelin 1 (ET-1) and human monocyte chemoattractant protein 1 (MCP-1), resulting in F-actin recombination and vinculin aggregation as well as endothelial cell migration. In vitro studies have shown that leptin leads to increased WNT1 expression and the accumulation of β-catenin. Metastasis-associated protein 1 (MTA1), a critical upstream modifier of WNT1 signaling, increased the expression level in leptin-mediated regulation. In contrast, opposite results were observed when cells are transfected with MTA1 or WNT1 shRNA lentivirus vectors. Among 160 patients with CKD and 160 healthy subjects, patients with CKD had significantly higher serum leptin levels than those of the control group, which were positively correlated with increased levels of IL-6, ET-1 and MCP-1. However, these levels were negatively correlated with flow-mediated dilatation (FMD). Hence, these investigations provided novel information on the increased serum leptin levels in CKD patients leading to ED via the MTA1-WNT/β-catenin pathway.

Indexed as

Wnt Signaling PathwayAdultbeta CateninEndothelium, VascularFemaleHumansHuman Umbilical Vein Endothelial CellsLeptinMaleMiddle AgedRenal Insufficiency, ChronicRepressor ProteinsTrans-Activatorsbeta CateninCTNNB1 protein, humanLEP protein, humanLeptinMTA1 protein, humanRepressor ProteinsTrans-ActivatorsChronic kidney diseaseEndothelial dysfunctionLeptinMetastasis-associated protein 1Wnt/β-catenin pathway

Identifiers

PMID32632610
OpenAlexW3039144507

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.