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Determination of the Relative Cell Surface and Total Expression of Recombinant Ion Channels Using Flow Cytometry
Published on: September 28, 2016
Ion channel trafficking implications in heart failure
Jean-Baptiste Reisqs1, Yongxia Sarah Qu1,2, Mohamed Boutjdir1,3,4
1Cardiovascular Research Program, VA New York Harbor Healthcare System, New York, NY, United States.
Insights
Heart failure (HF) involves ion channel dysfunction, particularly affecting sodium and potassium currents, leading to arrhythmias. Understanding ion channel trafficking offers new therapeutic avenues for HF treatment.
Area of Science:
- Cardiology
- Molecular Biology
- Electrophysiology
Background:
- Heart failure (HF) is a growing global epidemic, affecting millions and causing significant mortality and morbidity.
- Current HF therapies improve survival but cannot halt the rising incidence, necessitating a deeper understanding of underlying mechanisms.
- Arrhythmias are a serious complication of HF, stemming from electrophysiological changes in cardiomyocytes.
Purpose of the Study:
- To review recent advances in understanding ion channel trafficking in the context of heart failure.
- To highlight the role of ion channel trafficking defects in cardiomyocyte electrophysiology and arrhythmia development.
- To explore the potential of targeting ion channel trafficking for novel HF therapies.
Main Methods:
- Literature review focusing on ion channel trafficking mechanisms in heart failure.
- Analysis of molecular and cellular alterations impacting ion channel function and organization.
- Synthesis of current research on the relationship between ion channel trafficking and cardiac electrophysiology.
Main Results:
- Defects in ion channel trafficking, including alterations in sodium and potassium currents, are implicated in HF-related arrhythmias.
- Mechanisms such as variants, microtubule changes, and anchoring protein disturbances disrupt ion channel localization and function.
- Dysfunctional ion channel trafficking significantly alters cardiomyocyte electrophysiology, contributing to HF pathophysiology.
Conclusions:
- Ion channel trafficking is a critical determinant of cardiomyocyte electrophysiology and a key contributor to heart failure.
- Understanding these trafficking mechanisms provides a basis for developing innovative therapeutic strategies for HF.
- Targeting ion channel trafficking pathways may offer a novel approach to manage HF and its associated arrhythmias.
Abstract:
Heart failure (HF) is recognized as an epidemic in the contemporary world, impacting around 1%-2% of the adult population and affecting around 6 million Americans. HF remains a major cause of mortality, morbidity, and poor quality of life. Several therapies are used to treat HF and improve the survival of patients; however, despite these substantial improvements in treating HF, the incidence of HF is increasing rapidly, posing a significant burden to human health. The total cost of care for HF is USD 69.8 billion in 2023, warranting a better understanding of the mechanisms involved in HF. Among the most serious manifestations associated with HF is arrhythmia due to the electrophysiological changes within the cardiomyocyte. Among these electrophysiological changes, disruptions in sodium and potassium currents' function and trafficking, as well as calcium handling, all of which impact arrhythmia in HF. The mechanisms responsible for the trafficking, anchoring, organization, and recycling of ion channels at the plasma membrane seem to be significant contributors to ion channels dysfunction in HF. Variants, microtubule alterations, or disturbances of anchoring proteins lead to ion channel trafficking defects and the alteration of the cardiomyocyte's electrophysiology. Understanding the mechanisms of ion channels trafficking could provide new therapeutic approaches for the treatment of HF. This review provides an overview of the recent advances in ion channel trafficking in HF.
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