S100A1 gene therapy for heart failure: A novel strategy on the verge of clinical trials
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...
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| Main Authors: | , , , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
2011
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| In: |
Journal of molecular and cellular cardiology
Year: 2011, Volume: 50, Issue: 5, Pages: 777-784 |
| ISSN: | 1095-8584 |
| DOI: | 10.1016/j.yjmcc.2010.08.012 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.yjmcc.2010.08.012 Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S0022282810002993 
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| Author Notes: | David Rohde, Henriette Brinks, Julia Ritterhoff, Gang Qui, Shumei Ren, Patrick Most |
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| 520 | |a 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 cardiomyocyte 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”. | ||
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