Special Issue "Cardiac Calcium Channels in Cardiovascular Function and Disease"
Deadline for manuscript submissions: closed (20 July 2023) | Viewed by 179
Interests: signal transduction; cell culture; cell signaling; apoptosis; immunofluorescence; primary cell culture; cellular biology; signaling; cell imaging; in vitro cell culture
Interests: Caheart; arrhythmias; ischemia; heart failure; echocardiography; cardiac function; calcium; cardiomyopathies; cardiac electrophysiology
Calcium (Ca2+) signaling and the interacting networks regulate a plethora of cellular processes, such as gene expression, inflammation, synaptic transmission, induction of synaptic plasticity, excitation–contraction coupling, stimulus–secretion coupling or embryonic development.
This Special Issue will address the structure, function, and regulation of different types of Ca2+ channels in the heart as well as the consequences of their dysregulation, beginning with the L-type Ca2+ channels or dihydropyridine receptors (DHPR) at the cell membrane and the Ca release channels or ryanodine receptors (RyR2), at the sarcoplasmic reticulum (SR). These two Ca channels are main players in the process that, starting at the surface membrane level, ends inside the cell at the myofilaments level, to produce contraction, a mechanism known as excitation–contraction coupling (ECC). Alteration of this mechanism leads to cardiac arrhythmias, as well as different processes of cell death, such as apoptosis and necrosis.
In addition to these two main channels for ECC, a sophisticated system of channels and receptors is responsible for maintaining the Ca2+ concentration in cells within tight limits. This system includes the IP3 receptors, the different types of Transient Receptor Potential Canonical (TRPC) channels, as well as the Store Operated Ca channels (SOCE). This issue will also tackle these Ca2+ channels, their functional role and regulation, as well as their possible participation in different cardiac diseases.
The issue welcomes contributions that use animal, cellular, molecular and in silico approaches to shed light on pathophysiological mechanisms that involve Ca2+ channels and their impact on cardiac Ca2+ handling. Studies that have a translational perspective and contribute to closing the gap between health and disease through the modulation of Ca2+ channel function are of special interest.
Dr. Martin Vila Petroff
Prof. Dr. Alicia Mattiazzi
Manuscript Submission Information
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