Role of Ca2+ in healthy and pathologic cardiac function: from normal excitation–contraction coupling to mutations that cause inherited arrhythmia
Author:
Publisher
Springer Science and Business Media LLC
Subject
Health, Toxicology and Mutagenesis,Toxicology,General Medicine
Link
https://link.springer.com/content/pdf/10.1007/s00204-022-03385-0.pdf
Reference198 articles.
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2. Alsina KM, Hulsurkar M, Brandenburg S et al (2019) Loss of protein phosphatase 1 regulatory subunit PPP1R3A promotes atrial fibrillation. Circulation 140(8):681–693. https://doi.org/10.1161/CIRCULATIONAHA.119.039642
3. Altmann HM, Tester DJ, Will ML et al (2015) Homozygous/compound heterozygous triadin mutations associated with autosomal-recessive long-QT syndrome and pediatric sudden cardiac arrest: elucidation of the triadin knockout syndrome. Circulation 131(23):2051–2060. https://doi.org/10.1161/CIRCULATIONAHA.115.015397
4. Antzelevitch C, Pollevick GD, Cordeiro JM et al (2007) Loss-of-function mutations in the cardiac calcium channel underlie a new clinical entity characterized by ST-segment elevation, short QT intervals, and sudden cardiac death. Circulation 115(4):442–449. https://doi.org/10.1161/CIRCULATIONAHA.106.668392
5. Arvanitis DA, Vafiadaki E, Fan GC et al (2007) Histidine-rich Ca-binding protein interacts with sarcoplasmic reticulum Ca-ATPase. Am J Physiol Heart Circ Physiol 293(3):H1581–H1589. https://doi.org/10.1152/ajpheart.00278.2007
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