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Published on: July 5, 2021
Hypertension Induces Pro-arrhythmic Cardiac Connexome Disorders: Protective Effects of Treatment
Matus Sykora1, Katarina Andelova1, Barbara Szeiffova Bacova1
1Centre of Experimental Medicine, Slovak Academy of Sciences, Institute for Heart Research, 84104 Bratislava, Slovakia.
Insights
Arterial hypertension damages heart cell connections (connexomes), leading to arrhythmias and heart failure. Treatments may protect these vital connections, suggesting new therapeutic avenues for heart health.
Area of Science:
- Cardiovascular Science
- Cell Biology
- Hypertension Research
Background:
- Population aging and lifestyle factors drive increasing rates of arterial hypertension.
- Hypertension is linked to low-grade inflammation, heart dysfunction, and failure.
- Hypertension-induced changes promote atrial and ventricular fibrillation, increasing stroke and sudden death risks.
Purpose of the Study:
- To elucidate hypertension's detrimental effects on cardiomyocyte connexomes.
- To explore the role of connexome dysfunction in cardiac arrhythmias and heart failure.
- To review the impact of antihypertensive treatments on myocardial remodeling and connexome function.
Main Methods:
- Literature review on hypertension, cardiac remodeling, and connexome function.
- Analysis of studies investigating connexome impairment in hypertensive hearts.
- Examination of evidence regarding antihypertensive therapies and their effects on myocardial structure and connexomes.
Main Results:
- Hypertension impairs connexome integrity, crucial for cell adhesion and signal propagation.
- Connexome dysfunction is implicated as a key factor in cardiac arrhythmias and heart failure development.
- Antihypertensive treatments show potential to mitigate myocardial remodeling and preserve connexome function.
Conclusions:
- Connexome integrity is vital for maintaining normal heart function and preventing arrhythmias.
- Antihypertensive agents may possess pleiotropic effects, including anti-inflammatory actions, that protect connexomes.
- Further research is needed to identify molecular targets for connexome protection and develop novel heart failure therapies.
Abstract:
Prolonged population aging and unhealthy lifestyles contribute to the progressive prevalence of arterial hypertension. This is accompanied by low-grade inflammation and over time results in heart dysfunction and failure. Hypertension-induced myocardial structural and ion channel remodeling facilitates the development of both atrial and ventricular fibrillation, and these increase the risk of stroke and sudden death. Herein, we elucidate hypertension-induced impairment of "connexome" cardiomyocyte junctions. This complex ensures cell-to-cell adhesion and coupling for electrical and molecular signal propagation. Connexome dysfunction can be a key factor in promoting the occurrence of both cardiac arrhythmias and heart failure. However, the available literature indicates that arterial hypertension treatment can hamper myocardial structural remodeling, hypertrophy and/or fibrosis, and preserve connexome function. This suggests the pleiotropic effects of antihypertensive agents, including anti-inflammatory. Therefore, further research is required to identify specific molecular targets and pathways that will protect connexomes, and it is also necessary to develop new approaches to maintain heart function in patients suffering from primary or pulmonary arterial hypertension.
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