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Updated: Nov 8, 2025

Isolation of Mouse Interstitial Valve Cells to Study the Calcification of the Aortic Valve In Vitro
Published on: May 10, 2021
Role of oxidative stress in calcific aortic valve disease and its therapeutic implications
Harry Z E Greenberg1, Guoan Zhao2, Ajay M Shah1
1Department of Cardiology, Cardiovascular Division, King's College London British Heart Foundation Centre of Research Excellence, James Black Centre, 125 Coldharbour Lane, London SE5 9NU, UK.
Insights
Calcific aortic valve disease (CAVD) involves fibrosis and calcification. Oxidative stress from reactive oxygen species (ROS) drives CAVD, highlighting ROS as potential therapeutic targets for this condition.
Area of Science:
- Cardiovascular Medicine
- Pathophysiology
- Biochemistry
Background:
- Calcific aortic valve disease (CAVD) is a major cause of cardiovascular morbidity and mortality in Western populations.
- Aging populations are expected to increase the burden of CAVD.
- Currently, no effective pharmacological therapies exist to prevent, treat, or slow CAVD progression.
Purpose of the Study:
- To review the roles and sources of reactive oxygen species (ROS) in the pathophysiology of CAVD.
- To explore the potential of ROS as novel therapeutic targets for CAVD.
Main Methods:
- Literature review focusing on the mechanisms of CAVD.
- Analysis of the role of oxidative stress and ROS in valve interstitial cell differentiation.
- Examination of current research on therapeutic targets for CAVD.
Main Results:
- Reactive oxygen species (ROS)-mediated oxidative stress plays a significant causative role in CAVD.
- ROS induce the differentiation of valve interstitial cells into myofibroblasts and osteoblasts.
- Understanding ROS pathways is crucial for developing new treatments.
Conclusions:
- Oxidative stress driven by ROS is a key factor in the development and progression of CAVD.
- Targeting ROS presents a promising therapeutic strategy for managing CAVD.
- Further research into ROS mechanisms could lead to effective interventions.
Abstract:
Calcific aortic valve disease (CAVD) is the end result of active cellular processes that lead to the progressive fibrosis and calcification of aortic valve leaflets. In western populations, CAVD is a significant cause of cardiovascular morbidity and mortality, and in the absence of effective drugs, it will likely represent an increasing disease burden as populations age. As there are currently no pharmacological therapies available for preventing, treating, or slowing the development of CAVD, understanding the mechanisms underlying the initiation and progression of the disease is important for identifying novel therapeutic targets. Recent evidence has emerged of an important causative role for reactive oxygen species (ROS)-mediated oxidative stress in the pathophysiology of CAVD, inducing the differentiation of valve interstitial cells into myofibroblasts and then osteoblasts. In this review, we focus on the roles and sources of ROS driving CAVD and consider their potential as novel therapeutic targets for this debilitating condition.
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