Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

IL-6 promotes epithelial-to-mesenchymal transition of human peritoneal mesothelial cells possibly through the JAK2/STAT3 signaling pathway.

American journal of physiology. Renal physiology - 1 Aug 2017

Xiao Jing, Gong Yanan, Chen Ying, Yu Dahai, Wang Xiaoyang, Zhang Xiaoxue, Dou Yanna, Liu Dong, Cheng Genyang, Lu Shan, Yuan Wenming, Li Yansheng, Zhao Zhanzheng

Abstract excerpt

Long-term peritoneal dialysis (PD) therapy results in functional and structural alteration of the peritoneal membrane, including epithelial-to-mesenchymal transition (EMT). Interleukin 6 (IL-6) is a local pleiotropic cytokine, hypothesized to play an important role in EMT. This study was designed to investigate the role of IL-6 in EMT and peritoneal membrane dysfunction in long-term PD patients by assessing the...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cell Shape
Share to Epithelial-Mesenchymal Transition

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Janus Kinase 2

Share to Kidney Failure, Chronic

Share to Peritoneal Dialysis

Share to Peritoneum

Share to STAT3 Transcription Factor

Share to Vascular Endothelial Growth Factor A

Source

Identifiers

PMID: 28490530
DOI: 10.1152/ajprenal.00428.2016

Genes

JAK2
STAT3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

IL-6 promotes epithelial-to-mesenchymal transition of human peritoneal mesothelial cells possibly through the JAK2/STAT3 signaling pathway.PMID 28490530Read ↗

Inhibition of STAT3 by S3I-201 suppress peritoneal fibroblast phenotype conversion and alleviate peritoneal fibrosis.Semantic proximity Read ↗

Epithelial-to-mesenchymal transition of mesothelial cells is an early event during peritoneal dialysis and is associated with high peritoneal transport.Semantic proximity Read ↗

Inhibition of transforming growth factor-activated kinase 1 (TAK1) blocks and reverses epithelial to mesenchymal transition of mesothelial cells.Semantic proximity Read ↗

A pathogenetic role for endothelin-1 in peritoneal dialysis-associated fibrosis.Semantic proximity Read ↗

Blocking TGF-β1 protects the peritoneal membrane from dialysate-induced damage.Semantic proximity Read ↗

Genomic reprograming analysis of the Mesothelial to Mesenchymal Transition identifies biomarkers in peritoneal dialysis patientsSemantic proximity Read ↗

IL-6/STAT3/TFF3 signaling regulates human biliary epithelial cell migration and wound healing in vitroSemantic proximity Read ↗

Interleukin-6 at the Host-Tumor Interface: STAT3 in Biomolecular Condensates in Cancer CellsSemantic proximity Read ↗

p38 maintains E-cadherin expression by modulating TAK1-NF-kappa B during epithelial-to-mesenchymal transition.Semantic proximity Read ↗

Human peritoneal mesothelial cells produce many cytokines (granulocyte colony-stimulating factor [CSF], granulocyte-monocyte-CSF, macrophage-CSF, interleukin-1 [IL-1], and IL-6) and are activated and stimulated to grow by IL-1.Semantic proximity Read ↗

MiR-503-5p mediates cell cycle arrest and fibrosis of peritoneal mesothelial cells with a high peritoneal solute transport statusSemantic proximity Read ↗

Tamoxifen ameliorates peritoneal membrane damage by blocking mesothelial to mesenchymal transition in peritoneal dialysis.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.