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Wu, Y., MacMillan, L.B., McNeill, R.B., Colbran, R.J. and Anderson, M.E. (1999) Cam Kinase Augments Cardiac L-Type Ca²⁺ Current: A Cellular Mechanism for Long Q-T Arrhythmias. American Journal of Physiology-Heart and Circulatory Physiology, 276, H2168-H2178.
https://doi.org/10.1152/ajpheart.1999.276.6.h2168

has been cited by the following article:

• TITLE: Emerging Role of CaMKII as a Possible Therapeutic Target for Cardiovascular Diseases

  AUTHORS: Suvechha Bhandari, Terry Oroszi

  KEYWORDS: CaMKII, Cardiovascular Diseases, Heart Failure, Arrhythmias, Diabetes, Inflammation, Cardiac Remodeling, Ion Channels, Therapeutic Target, Drug Development

  JOURNAL NAME: World Journal of Cardiovascular Surgery, Vol.14 No.12, December 30, 2024

  ABSTRACT: Calcium/calmodulin-dependent protein kinase II (CaMKII) is a key regulator of heart function. While some CaMKII activity is beneficial, excessive, or persistent, CaMKII can lead to heart damage. CaMKII is often elevated in conditions like diabetes and heart disease, contributing to various cardiovascular problems. Therefore, CaMKII is considered a potential target for drug therapy, although its complex nature poses challenges. This review summarizes the structure, regulation, and roles of CaMKII in both normal and disease states, mainly focusing on its involvement in heart problems.