Related Experiment Video
Updated: Sep 20, 2025

Isolation and Characterization of Primary Rat Valve Interstitial Cells: A New Model to Study Aortic Valve Calcification
Published on: November 20, 2017
Knockdown of PARM1 Alleviates Aortic Valve Calcification via the PRKCH-MAPK Signaling Pathway
Haochang Hu1, Xian Zhu2, Jinyong Chen1
1Department of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China; State Key Laboratory of Transvascular Implantation Devices, Hangzhou, Zhejiang, China; Heart Regeneration and Repair Key Laboratory of Zhejiang Province, Hangzhou, Zhejiang, China.
Abstract:
With the aging of the population, the prevalence of calcific aortic valve disease (CAVD) has increased yearly. However, effective means to delay or even reverse the progression of CAVD are still lacking. This study revealed that prostate androgen-regulated mucin-like protein 1 (PARM1) expression was significantly up-regulated in calcified aortic valve tissues. Functional investigations demonstrated that PARM1 knockdown effectively suppressed osteogenic differentiation of valvular interstitial cells (VICs) and mitigated pathological aortic valve calcification. Mechanically, PARM1 knockdown down-regulated PRKCH mRNA expression, consequently attenuating MAPK pathway activation during the osteogenic differentiation of VICs. In conclusion, PARM1 could be a feasible target for CAVD prevention.
Insights
Prostate androgen-regulated mucin-like protein 1 (PARM1) is elevated in calcific aortic valve disease (CAVD). Targeting PARM1 suppressed valve calcification by inhibiting osteogenic differentiation of valvular interstitial cells.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Biomaterials Science
Background:
- Calcific aortic valve disease (CAVD) prevalence increases with population aging.
- Current treatments for CAVD lack methods to delay or reverse disease progression.
- Valvular interstitial cells (VICs) play a critical role in CAVD pathogenesis.
Purpose of the Study:
- To investigate the role of prostate androgen-regulated mucin-like protein 1 (PARM1) in CAVD.
- To determine if PARM1 is a potential therapeutic target for CAVD.
Main Methods:
- Analysis of PARM1 expression in human calcified aortic valve tissues.
- In vitro studies involving PARM1 knockdown in VICs.
- Investigation of downstream signaling pathways, including PRKCH mRNA and MAPK activation.
Main Results:
- PARM1 expression was significantly upregulated in calcified aortic valve tissues.
- PARM1 knockdown suppressed VIC osteogenic differentiation and mitigated aortic valve calcification.
- PARM1 knockdown led to decreased PRKCH mRNA expression and attenuated MAPK pathway activation.
Conclusions:
- PARM1 is a key mediator in the osteogenic differentiation of VICs and CAVD progression.
- PARM1 represents a potential therapeutic target for preventing or treating CAVD.

