Ca2+ mishandling in heart failure: Potential targets
Almudena Val-Blasco1, Marta Gil-Fernández1, Angélica Rueda2
1La Paz University Hospital Health Research Institute, IdiPAZ, Madrid, Spain.
Insights
Calcium (Ca2+) mishandling contributes to heart failure (HF) progression. Novel research highlights the roles of the immune system, bone metabolism, and protein modifications in Ca2+ regulation and HF development.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Physiology
Background:
- Calcium (Ca2+) mishandling is a hallmark of cardiovascular diseases, including heart failure (HF).
- Dysregulation of intracellular Ca2+ homeostasis underlies cardiac dysfunction and arrhythmias in HF.
- Understanding Ca2+ handling is crucial for developing effective HF therapies.
Purpose of the Study:
- To review novel findings on Ca2+ mishandling in heart failure progression.
- To identify emerging targets regulating Ca2+ handling in HF.
- To explore the contribution of new areas to HF pathogenesis.
Main Methods:
- Literature review of recent research studies on Ca2+ handling in HF.
- Analysis of emerging areas implicated in Ca2+ regulation.
- Synthesis of findings on the role of the innate immune system, bone metabolism, and post-translational modifications.
Main Results:
- Ca2+ mishandling is a central mechanism in HF.
- Emerging research identifies the innate immune system as a key regulator of Ca2+ handling in HF.
- Bone metabolism factors and post-translational modifications of proteins also significantly impact Ca2+ regulation in HF progression.
Conclusions:
- Novel therapeutic targets for HF may lie in modulating Ca2+ handling.
- The innate immune system, bone metabolism, and protein modifications represent promising areas for future HF research.
- Further investigation into these areas could lead to improved treatments for heart failure.
Abstract:
Ca2+ mishandling is a common feature in several cardiovascular diseases such as heart failure (HF). In many cases, impairment of key players in intracellular Ca2+ homeostasis has been identified as the underlying mechanism of cardiac dysfunction and cardiac arrhythmias associated with HF. In this review, we summarize primary novel findings related to Ca2+ mishandling in HF progression. HF research has increasingly focused on the identification of new targets and the contribution of their role in Ca2+ handling to the progression of the disease. Recent research studies have identified potential targets in three major emerging areas implicated in regulation of Ca2+ handling: the innate immune system, bone metabolism factors and post-translational modification of key proteins involved in regulation of Ca2+ handling. Here, we describe their possible contributions to the progression of HF.
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