Evidence map›Paper›PMID 37233949›Full record

ArticlePharmacological reports : PR2023

Soluble dipeptidyl peptidase-4 induces epithelial-mesenchymal transition through tumor growth factor-β receptor.

Cheng-Wei Huang, Shih-Yi Lee, Chen-Xuan Du, Hui-Chun Ku

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Article in Pharmacological reports : PR, 2023. 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
1.4field-weighted citation impact, top 16% 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, 6 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Cheng-Wei Huang *Department of Life Science, Fu Jen Catholic University, No.510, Zhongzheng Road, Xinzhuang District, New Taipei City, 242, Taiwan.
Shih-Yi Lee *Division of Pulmonary and Critical Care Medicine, MacKay Memorial Hospital, Taipei, Taiwan.
Chen-Xuan DuDepartment of Life Science, Fu Jen Catholic University, No.510, Zhongzheng Road, Xinzhuang District, New Taipei City, 242, Taiwan.
Hui-Chun KuDepartment of Life Science, Fu Jen Catholic University, No.510, Zhongzheng Road, Xinzhuang District, New Taipei City, 242, Taiwan. 141655@mail.fju.edu.tw.
Fu Jen Catholic University · TWMackay Junior College of Medicine, Nursing and Management · TW

Funding

Ministry of Science and Technology, Taiwan 109-2320-B-030-006-MY3
6 · The paper itself

Abstract

backgroundKidney fibrosis is the final manifestation of chronic kidney disease, a condition mainly caused by diabetic nephropathy. Persistent tissue damage leads to chronic inflammation and excessive deposition of extracellular matrix (ECM) proteins. Epithelial-mesenchymal transition (EMT) is involved in a variety of tissue fibrosis and is a process during which epithelial cells transform into mesenchymal-like cells and lose their epithelial functionality and characteristics Dipeptidyl peptidase-4 (DPP4) is widely expressed in tissues, especially those of the kidney and small intestine. DPP4 exists in two forms: a plasma membrane-bound and a soluble form. Serum-soluble DPP4 (sDPP4) levels are altered in many pathophysiological conditions. Elevated circulating sDPP4 is correlated with metabolic syndrome. Because the role of sDPP4 in EMT remains unclear, we examined the effect of sDPP4 on renal epithelial cells.

methodsThe influences of sDPP4 on renal epithelial cells were demonstrated by measuring the expression of EMT markers and ECM proteins.

resultssDPP4 upregulated the EMT markers ACTA2 and COL1A1 and increased total collagen content. sDPP4 activated SMAD signaling in renal epithelial cells. Using genetic and pharmacological methods to target TGFBR, we observed that sDPP4 activated SMAD signaling through TGFBR in epithelial cells, whereas genetic ablation and treatment with TGFBR antagonist prevented SMAD signaling and EMT. Linagliptin, a clinically available DPP4 inhibitor, abrogated sDPP4-induced EMT.

conclusionsThis study indicated that sDPP4/TGFBR/SMAD axis leads to EMT in renal epithelial cells. Elevated circulating sDPP4 levels may contribute to mediators that induce renal fibrosis.

Indexed as

Epithelial-Mesenchymal TransitionNeoplasmsDipeptidyl Peptidase 4FibrosisHumansTransforming Growth Factor betaTransforming Growth Factor beta1Dipeptidyl Peptidase 4Transforming Growth Factor betaTransforming Growth Factor beta1Epithelial–mesenchymal transitionSoluble dipeptidyl peptidase-4Suppressor of mothers against decapentaplegicTransforming growth factor-β receptor

Identifiers

PMID37233949
OpenAlexW4378348954

What Socratic holds

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Registered trials

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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 Socratic graph.