Journal
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
Volume 50, Issue 5, Pages 777-784Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2010.08.012
Keywords
S100A1; Gene therapy; Heart failure; Calcium; Sarcoplasmic; Reticulum; Myofilaments; Mitochondria
Categories
Funding
- National Institute of Health [RO1 HL92130, RO1 HL92130-02 S1]
- Deutsche Forschungsgemeinschaft [562/1-1]
- Bundesministerium fuer Bildung und Forschung [01GU0572]
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Representing the common endpoint of various cardiovascular disorders, heart failure (HF) shows a dramatically growing prevalence. As currently available therapeutic strategies are not capable of terminating the progress of the disease, HF is still associated with a poor clinical prognosis. Among the underlying molecular mechanisms, the loss of cardiomyocyte Ca2+ cycling integrity plays a key role in the pathophysiological development and progression of the disease. The cardiornyocyte EF-hand Ca2+ sensor protein S100A1 emerged as a regulator both of sarcoplasmic reticulum (SR), sarcomere and mitochondrial function implicating a significant role in cardiac physiology and dysfunction. In this review, we aim to recapitulate the translation of S100A1-based investigation from first clinical observations over basic research experiments back to a near-clinical setting on the verge of clinical trials today. We also address needs for further developments towards second-generation gene therapy and discuss the therapeutic potential of S100A1 gene therapy for HF as a promising novel strategy for future cardiologists. This article is part of a Special Section entitled Special Section: Cardiovascular Gene Therapy. (C) 2010 Elsevier Ltd. All rights reserved.
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