STIM1-dependent Store-Operated Ca2+ Entry is Required for Pathological Cardiac Hypertrophy

摘要

BackgroundAlterations in intracellular Ca²⁺ homeostasis are an important trigger of pathological cardiac remodeling; however, mechanisms governing context-dependent changes in Ca²⁺ influx are poorly understood. Store-operated Ca²⁺ entry (SOCE) is a major mechanism regulating Ca²⁺ trafficking in numerous cell types, yet its prevalence in adult heart and possible role in physiology and disease are each unknown. The Ca²⁺-binding protein, stromal interaction molecule 1 (STIM1), is a Ca²⁺ sensor in the sarcoplasmic reticulum (SR), capable of triggering SOCE by interacting with plasma membrane Ca²⁺ channels.