Key result
Recent advances in cardiac physiology highlight the complex interplay of CaMKII, nitric oxide, reactive oxygen species, and T-tubule disturbances in regulating cardiac contractility and arrhythmogenesis.
This review provides a comprehensive overview of recent basic science discoveries regarding the molecular mechanisms of cardiac contractility and their implications for heart failure and arrhythmogenesis.
These molecular insights remain preclinical; leaves open targeted trials before informing HF or arrhythmia management.
The aim of this review is to provide the reader with a synopsis of some of the emerging ideas and experimental findings in cardiac physiology and pathophysiology that were published in 2015. To provide context for the non-specialist, a brief summary of cardiac contraction and calcium (Ca) regulation in the heart in health and disease is provided. Thereafter, some recently published articles are introduced that indicate the current thinking on (1) the Ca regulatory pathways modulated by Ca/calmodulin-dependent protein kinase II, (2) the potential influences of nitrosylation by nitric oxide or S-nitrosated proteins, (3) newly observed effects of reactive oxygen species (ROS) on contraction and Ca regulation following myocardial infarction and a possible link with changes in mitochondrial Ca, and (4) the effects of some of these signaling pathways on late Na current and pro-arrhythmic afterdepolarizations as well as the effects of transverse tubule disturbances.
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Ken MacLeod (2016) conducted a review in Heart failure and arrhythmias. Recent advances in cardiac physiology highlight the complex interplay of CaMKII, nitric oxide, reactive oxygen species, and T-tubule disturbances in regulating cardiac contractility and arrhythmogenesis.
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