S100A1 gene therapy for heart failure: a novel strategy on the verge of clinical trials

Rohde, David; Brinks, Henriette; Ritterhoff, Julia; Qui, Gang; Ren, Shumei; Most, Patrick (2011). S100A1 gene therapy for heart failure: a novel strategy on the verge of clinical trials. Journal of molecular and cellular cardiology, 50(5), pp. 777-84. Oxford: Elsevier 10.1016/j.yjmcc.2010.08.012

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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 Ca(2+) cycling integrity plays a key role in the pathophysiological development and progression of the disease. The cardiomyocyte EF-hand Ca(2+) 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".

Item Type:

Journal Article (Original Article)


04 Faculty of Medicine > Department of Cardiovascular Disorders (DHGE) > Clinic of Cardiovascular Surgery

UniBE Contributor:

Most, Henriette


600 Technology > 610 Medicine & health








Factscience Import

Date Deposited:

04 Oct 2013 14:13

Last Modified:

05 Dec 2022 14:02

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Web of Science ID:



https://boris.unibe.ch/id/eprint/2749 (FactScience: 205623)

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