Background: In heart failure, the release of calcium becomes erratic leading to the generation of arrhythmias. Dysregulated Zn2+ homeostasis occurs in chronic heart failure.Results: Zn2+ can directly activate RyR2, removing the dependence of Ca2+ for channel activation.Conclusion: Zn2+ shapes Ca2+ dynamics by directly interacting with and modulating RyR2 function.Significance: This highlights a new role for Zn2+ in cardiac excitation-contraction coupling.
Zinc homeostasis is essential for normal cellular function, and defects in this process are associated with a number of diseases including type 2 diabetes (T2D), neurological disorders and cardiovascular disease. Thus, variants in the SLC30A8 gene, encoding the vesicular/granular zinc transporter ZnT8, are associated with altered insulin release and increased T2D risk while the zinc importer ZIP12 is implicated in pulmonary hypertension. In light of these, and findings in other diseases, recent efforts have focused on the development of refined sensors for intracellular free zinc ions that can be targeted to subcellular regions including the cytosol, endoplasmic reticulum (ER), secretory granules, Golgi apparatus, nucleus and the mitochondria. Here, we discuss recent advances in Zn probe engineering and their applications to the measurement of labile subcellular zinc pools in different cell types.
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