Microtubule-Mediated Defects in Junctophilin-2 Trafficking Contribute to Myocyte T-Tubule Remodeling and Ca Handling Dysfunction in Heart Failure

نویسندگان

  • Caimei Zhang
  • Yanqi Zhu
  • Jordan D. Miller
  • Robert M. Weiss
  • Xander H. T. Wehrens
  • Frances L. Johnson
  • Luis F. Santana
  • Mark E. Anderson
  • Long-Sheng Song
چکیده

Division of Cardiovascular Medicine, Dept of Internal Medicine, University of Iowa Carver College of Medicine, Iowa City, IA; Shanghai First People’s Hospital, Shanghai Jiaotong University, Shanghai, China; Division of Cardiovascular Surgery, Mayo Clinic, Rochester, MN; Dept of Pharmacology, College of Basic Medicine, Anhui Medical University, Hefei, China; Dept of Physiology & Biophysics, University of Washington School of Medicine, Seattle, WA; Dept of Veterans Affairs Medical Center, Iowa City, IA; Dept of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX; Dept of Molecular Physiology and Biophysics, University of Iowa Carver College of Medicine, Iowa City, IA

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Microtubule-mediated defects in junctophilin-2 trafficking contribute to myocyte transverse-tubule remodeling and Ca2+ handling dysfunction in heart failure.

BACKGROUND Cardiac dysfunction in failing hearts of human patients and animal models is associated with both microtubule densification and transverse-tubule (T-tubule) remodeling. Our objective was to investigate whether microtubule densification contributes to T-tubule remodeling and excitation-contraction coupling dysfunction in heart disease. METHODS AND RESULTS In a mouse model of pressur...

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BACKGROUND A highly organized transverse tubule (T-tubule) network is necessary for efficient Ca(2+)-induced Ca(2+) release and synchronized contraction of ventricular myocytes. Increasing evidence suggests that T-tubule remodeling due to junctophilin-2 (JP-2) downregulation plays a critical role in the progression of heart failure. However, the mechanisms underlying JP-2 dysregulation remain i...

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تاریخ انتشار 2014