Premium
Role of the cytoskeleton in communication between L ‐type C a 2+ channels and mitochondria
Author(s) -
Viola Helena M,
Hool Livia C
Publication year - 2013
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12072
Subject(s) - cytoskeleton , mitochondrion , microbiology and biotechnology , oxidative phosphorylation , voltage dependent anion channel , myocyte , biology , organelle , chemistry , biochemistry , cell , bacterial outer membrane , escherichia coli , gene
Summary The L ‐type C a 2+ channel is the main route for C a 2+ entry into cardiac myocytes, which is essential for the maintenance of cardiac excitation and contraction. Alterations in L ‐type C a 2+ channel activity and C a 2+ homeostasis have been implicated in the development of cardiomyopathies. Cardiac excitation and contraction is fuelled by ATP , synthesized predominantly by the mitochondria via the C a 2+ ‐dependent process oxidative phosphorylation. Mitochondrial reactive oxygen species ( ROS ) are by‐products of oxidative phosphorylation and are associated with the development of cardiac pathology. The cytoskeleton plays a role in the communication of signals from the plasma membrane to intracellular organelles. There is good evidence that both L ‐type C a 2+ channel activity and mitochondrial function can be modulated by changes in the cytoskeletal network. Activation of the L ‐type C a 2+ channel can regulate mitochondrial function through cytoskeletal proteins as a result of transmission of movement from the β 2 ‐subunit of the channel that occurs during activation and inactivation of the channel. An association between cytoskeletal proteins and the mitochondrial voltage‐dependent anion channel ( VDAC ) may play a role in this response. The L ‐type C a 2+ channel is the initiator of contraction in cardiac muscle and the VDAC is responsible for regulating mitochondrial ATP / ADP trafficking. This article presents evidence that a functional coupling between L ‐type C a 2+ channels and mitochondria may assist in meeting myocardial energy demand on a beat‐to‐beat basis.