Cardiomyopathy at the Sub-cellular Level II

Dear Colleagues,

This Special Issue of JCDD is focused on “Cardiomyopathy at the Sub-cellular Level”, encompassing the molecular mechanisms of pathological remodeling within cardiomyocytes that lead to mechanical and electrical perturbation of the heart. Critical cardiomyocyte structures and nano-domains effect efficient excitation–contraction coupling (e.g., T-tubules, dyads, sarcomere) and intercellular action potential propagation (e.g., intercalated discs, gap junctions). Elegant genetic, biochemical, and imaging studies have revealed surprisingly dynamic regulation and turnover within such structures, rendering them subject to rapid alterations during stress and affecting their function. Population of cardiomyocyte subdomains with appropriate functional proteins is essential, with increasing studies finding that failure to deliver and/or maintain specific proteins within precise sub-cellular locations is a major cause of compromised cardiomyocyte function. Cellular regulatory hubs that have received substantial historical attention include altered gene expression at the transcriptional level and posttranslational modification of proteins. More recently, processes previously thought of as ‘constitutive’ such as post-transcriptional regulation at the point of protein translation and trafficking of de novo proteins within cardiomyocytes have been uncovered as highly dynamic and subject to pathological changes in diseased hearts. As our understanding grows, a clearer picture of the ‘healthy’ versus ‘diseased’ cardiomyocyte is emerging which, while complex, is unveiling new avenues for therapeutic intervention.

This Special Issue aims to collect articles related to the molecular mechanism of efficient excitation–contraction coupling at the sub-cellular level in cardiomyopathy and the pathological changes in the transcription and translation of functional proteins in cardiomyocytes.

Dr. James Smyth
Guest Editor

Manuscript Submission Information

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• T-tubule
• sarcomere
• transcription
• translation
• trafficking
• cytoskeleton
• ion channel
• intercalated disc
• connexin
• stress