Bridging integrator 1 Overview
Bridging integrator 1 is a membrane scaffolding/adaptor protein encoded by the BIN1 gene. The cardiac-specific isoform (“cardiac bridging integrator 1” or cBIN1) plays an essential role in organizing transverse tubule microdomains within cardiomyocytes that are critical for normal calcium handling during each heartbeat. Loss or reduction of cBIN1 disrupts these structures leading to impaired excitation-contraction coupling—a hallmark feature seen in various forms of heart failure. In addition to its structural role, BIN1 acts as a central signaling hub interacting with multiple proteins important for muscle cell function. Mutations or altered splicing can cause skeletal muscle diseases such as centronuclear myopathy and have been linked epidemiologically with Alzheimer’s disease. In cardiovascular medicine, decreased myocardial or circulating levels of cBIN1 correlate strongly with adverse ventricular remodeling and poor outcomes; thus it serves both as a promising biomarker (“cBINI score”) for diagnosis/prognosis—especially HFpEF—and an emerging therapeutic target via gene replacement strategies currently advancing toward clinical trials.
Mechanism of Action
Gene therapy to restore or augment cBIN1 expression aims to normalize t-tubule structure, improve calcium handling microdomains, reverse maladaptive remodeling, and rescue cardiac function in failing hearts by acting as a scaffold for key signaling proteins involved in excitation-contraction coupling
Biological Functions
Disease Associations
Safety Considerations
- As gene therapy is the main therapeutic approach under development, potential concerns include immune response to viral vectors such as AAV9, off-target effects, long-term safety/efficacy unknown at this stage. No major adverse effects reported so far in animal models but human data are pending.
Interacting Drugs
Associated Biomarkers
Biomarker |
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Plasma cBIN1 level (“cBIN1 score” or CS): a biomarker for diagnosis and monitoring of heart failure with preserved ejection fraction (HFpEF) and potentially other forms of cardiomyopathy. Lower plasma levels indicate greater risk/severity due to maladaptive remodeling. |