Circ Res 2016 Sep 29;119(8):944-55. Epub 2016 Aug 29.
From the Department of Cardiovascular Sciences, Imperial Centre for Translational and Experimental Medicine, National Heart and Lung Institute (J.L.S.-A., A.B., A.V.G., S.S., N.B., M.B.S., C.M., A.R.L., P.P.P., J.G.), Department of Medicine (Y.E.K.), and Department of Cardiothoracic Surgery, Hammersmith Hospital, National Heart and Lung Institute (P.P.P.), Imperial College London, United Kingdom; Department of Biomedical Engineering and Institute for Computational Medicine, Johns Hopkins University, Baltimore, MD (T.O., N.A.T.); NIHR Cardiovascular Biomedical Research Unit, Royal Brompton Hospital, London, United Kingdom (A.R.L.); Institute of Experimental Cardiovascular Research, University Medical Center Hamburg-Eppendorf, Hamburg, Germany (S.S., V.O.N.); and Department of Biotechnology, Indian Institute of Technology Hyderabad, Kandi, Telangana, India (A.B.).
Rationale: Disruption in subcellular targeting of Ca(2+) signaling complexes secondary to changes in cardiac myocyte structure may contribute to the pathophysiology of a variety of cardiac diseases, including heart failure (HF) and certain arrhythmias.
Objective: To explore microdomain-targeted remodeling of ventricular L-type Ca(2+) channels (LTCCs) in HF.
Methods And Results: Super-resolution scanning patch-clamp, confocal and fluorescence microscopy were used to explore the distribution of single LTCCs in different membrane microdomains of nonfailing and failing human and rat ventricular myocytes. Read More