Evidence map›Paper›PMID 36233032›Full record

ArticleInternational journal of molecular sciences2022

KITLG Promotes Glomerular Endothelial Cell Injury in Diabetic Nephropathy by an Autocrine Effect.

Jiun-Chi Huang, Szu-Chia Chen, Wei-An Chang, Wei-Wen Hung, Ping-Hsun Wu, Ling-Yu Wu, Jer-Ming Chang, Ya-Ling Hsu, Yi-Chun Tsai

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
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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

9 authors at 1 institution in 1 country.

Jiun-Chi HuangDepartment of Internal Medicine, Kaohsiung Municipal Siaogang Hospital, Kaohsiung Medical University, Kaohsiung 812, Taiwan.ORCID 0000-0002-5897-2860
Szu-Chia ChenDepartment of Internal Medicine, Kaohsiung Municipal Siaogang Hospital, Kaohsiung Medical University, Kaohsiung 812, Taiwan.
Wei-An ChangDivision of Pulmonary and Critical Care Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 807, Taiwan.ORCID 0000-0002-0049-5758
Wei-Wen HungDivision of Endocrinology and Metabolism, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 807, Taiwan.
Ping-Hsun WuSchool of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan.ORCID 0000-0003-1021-8161
Ling-Yu WuGraduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan.
Jer-Ming ChangSchool of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan.
Ya-Ling HsuDrug Development and Value Creation Research Center, Kaohsiung Medical University, Kaohsiung 807, Taiwan.
Yi-Chun TsaiSchool of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan.
Kaohsiung Medical University · TW

Funding

Kaohsiung Medical University Hospital KMUH 110-0R29Kaohsiung Municipal Siaogang Hospital H-110-007Ministry of Science and Technology, Taiwan MOST 108-2314-B-037-035-MY3Ministry of Science and Technology, Taiwan MOST 110-2314-B-037-036
6 · The paper itself

Abstract

Diabetic nephropathy (DN) is an increasing threat to human health. The impact of hyperglycemia or its metabolites, advanced glycation end-products (AGEs), on glomerular endothelial cells (GECs) and their pathophysiologic mechanisms are not well explored. Our results reveal that AGEs increased the expression and secretion of the KIT ligand (KITLG) in GECs. Both AGEs and KITLG promoted endothelial-to-mesenchymal transition (EndoMT) in GECs and further increased the permeability of GECs through the AKT/extracellular-signal-regulated kinase pathway. Inhibition of KITLG's effects by imatinib prevented AGE-medicated EndoMT in GECs, supporting the belief that KITLG is a critical factor for GEC injury. We found higher KITLG levels in the GECs and urine of db/db mice compared with db/m mice, and urinary KITLG levels were positively correlated with the urinary albumin-to-creatinine ratio (ACR). Furthermore, type 2 diabetic patients had higher urinary KITLG levels than normal individuals, as well as urinary KITLG levels that were positively correlated with urinary ACR and negatively correlated with the estimated glomerular filtration rate. KITLG plays a pathogenic role in GEC injury in DN and might act as a biomarker of DN progression.

Indexed as

Diabetes MellitusDiabetic NephropathiesStem Cell FactorAlbuminsAnimalsBiomarkersCreatinineEndothelial CellsHumansImatinib MesylateKidney GlomerulusMiceMice, Inbred StrainsProto-Oncogene Proteins c-aktAlbuminsBiomarkersCreatinineImatinib MesylateKITLG protein, humanProto-Oncogene Proteins c-aktStem Cell Factoradvanced glycation end-productsbiomarkerdiabetic nephropathyendothelial–to–mesenchymal transitionglomerular endothelial cellKITLG

Identifiers

PMID36233032
PMCPMC9569900
OpenAlexW4303699764

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.