Ca2+ mishandling in heart failure: Potential targets

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.

Keywords: EC coupling; calcium handling; heart failure; ryanodine.