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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Hauptverfasser: Rohde, David (VerfasserIn) , Brinks, Henriette (VerfasserIn) , Ritterhoff, Julia (VerfasserIn) , Qui, Gang (VerfasserIn) , Ren, Shumei (VerfasserIn) , Most, Patrick (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 2011
In: Journal of molecular and cellular cardiology
Year: 2011, Jahrgang: 50, Heft: 5, Pages: 777-784
ISSN:1095-8584
DOI:10.1016/j.yjmcc.2010.08.012
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.yjmcc.2010.08.012
Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S0022282810002993
Volltext
Verfasserangaben: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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