Related Experiment Video
Updated: Aug 6, 2026
07:31
Isolation of Human Primary Valve Cells for In vitro Disease Modeling
Published on: April 16, 2021
IL-17-associated Pro-inflammatory Programs in Aortic Valve Interstitial Cell Osteogenic Differentiation: JUN as a
Yining Dai1, Siyu Kong1, Yupeng Yang1
1Department of Cardiology, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, 510080, China.
Inflammation
|July 21, 2026
Summary
Interleukin-17 (IL-17) inflammation promotes calcific aortic valve disease (CAVD) by activating the JUN pathway in valvular cells. Inhibiting JUN reduces valve calcification, offering new therapeutic targets for CAVD.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Inflammation Research
Background:
- Calcific aortic valve disease (CAVD) is characterized by valve calcification, involving osteogenic differentiation of valvular interstitial cells (VICs).
- The precise molecular mechanisms linking inflammatory pathways to VIC osteogenesis in CAVD remain incompletely understood.
Purpose of the Study:
- To investigate the role of the interleukin-17 (IL-17) pathway in the osteogenic differentiation of human VICs.
- To identify key regulatory nodes connecting IL-17 signaling to VIC osteogenic programs.
Main Methods:
- Utilized an IL-17 pathway-guided transcriptomic strategy in human VIC osteogenic differentiation models.
- Performed RNA sequencing, functional enrichment, and multilayer network analyses.
- Validated findings through in vitro experiments and a mouse model of chronic kidney disease-induced CAVD.
Main Results:
- An IL-17-associated transcriptional program, enriched for MAPK pathways, was activated during VIC osteogenic differentiation.
- The transcription factor JUN was identified as a central node, upregulated during VIC osteogenesis and crucial for calcification.
- IL-17A stimulation enhanced VIC calcification, partially mediated by JUN, and JNK inhibition reduced calcification in a mouse model.
Conclusions:
- IL-17-associated inflammation is activated during VIC osteogenic differentiation and promotes CAVD.
- The JUN pathway is a key mediator linking IL-17 signaling to VIC osteogenic transcription and calcification.
- Targeting the IL-17/JUN axis presents a potential therapeutic strategy for CAVD.
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