Editorial: Ion transporters and channels in cellular pathophysiology

Editorial on the Research Topic Ion transporters and channels in cellular pathophysiologyIon and water channels and transporters mediate the flux of ions, water, and smalland medium-size molecules across cellular membranes in response to specific stimuli.Ion transport is crucial for proper cell, tissue, and organ function, including the regulation of cardiac and neuronal activity, systemic pH, salt and water homeostasis, as well as cell proliferation, differentiation, and apoptosis.As a consequence, the impairment of any of its molecular components may have dramatic consequences for cellular and organ physiology, and eventually for human health.Therefore, the precise understanding of the mechanisms of physiological regulation and pathological dysregulation of ion transport is essential to open new avenues in therapy and drug design.The purpose of this Research Topic was to collect and contribute to the dissemination of high-quality research articles summarizing the current progress in the understanding of different aspects of ion channels and transporters, including intracellular signaling.The 10 original publications collected are well representative of the variety of roles of ion channels and transporters and highlight the multitude of the experimental models and approaches currently used to unravel their complexity.Hereafter we offer an overview of the content of the Research Topic.Alterations in the ion transport can cause serious diseases affecting the heart and the central nervous system.Among these, sudden cardiac arrest (SCA) is a global public health problem.Most cases of SCA are caused by cardiac arrhythmias that may arise from functional changes of ion channels that underlie the cardiac action potential (AP) and can be evoked by various drugs used for the treatment of cardiac or non-cardiac conditions, including carbamazepine (CBZ).In their manuscript, Jia et al. showed a correlation between CBZ treatment and SCA and demonstrated that CBZ reduced the AP upstroke velocity by reducing the cardiac Na + current at therapeutic concentrations and shortened