S100A1: Another Step Toward Therapeutic Development for Heart Failure.

It has been nearly 130 years since Sydney Ringer’s astute observations on the indispensability of extracellular Ca to eart muscle contraction (1). At the cellular level, we now now that fluctuations of cytosolic Ca are coordinated by everal myocyte proteins in order to functionally couple the ardiac action potential to sarcomeric shortening and mitohondrial energy production. This elegant myocardial Ca cycling demands precise regulation of intracellular Ca , as videnced by the numerous examples of cardiac dysfunction rising from altered expression or activity of Ca handling roteins (2–5). One such protein, S100A1, has attracted the nterest of cardiac scientists because of its myocardial nrichment, known interactions with several other Ca