Key result
Review identifies innate immunity and bone metabolism as potential Ca2+ handling targets in heart failure.
Why the study?
Ca2+ mishandling underlies cardiac dysfunction and arrhythmias in heart failure, motivating a focus on novel targets regulating Ca2+ handling in disease progression.
This review highlights emerging targets for heart failure therapy focused on correcting intracellular calcium mishandling, specifically involving the innate immune system, bone metabolism factors, and post-translational modifications.
Potential targets for Ca2+ handling in heart failure require validation before clinical consideration; leaves open whether innate immune or bone metabolism modulation improves outcomes.
Ca 2+ mishandling is a common feature in several cardiovascular diseases such as heart failure (HF). In many cases, impairment of key players in intracellular Ca 2+ 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 Ca 2+ mishandling in HF progression. HF research has increasingly focused on the identification of new targets and the contribution of their role in Ca 2+ handling to the progression of the disease. Recent research studies have identified potential targets in three major emerging areas implicated in regulation of Ca 2+ handling: the innate immune system, bone metabolism factors and post‐translational modification of key proteins involved in regulation of Ca 2+ handling. Here, we describe their possible contributions to the progression of HF.
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Val‐Blasco et al. (2021) conducted a review in Heart failure. Potential targets in Ca2+ handling (innate immune system, bone metabolism factors, post-translational modifications) was evaluated. Recent research identifies potential targets for regulating Ca2+ handling in heart failure progression, including the innate immune system, bone metabolism factors, and post-translational modifications.
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