TY  - JOUR
A1  - Hou, Yunlong
A1  - Adrian-Segarra, Juan M.
A1  - Richter, Manfred
A1  - Kubin, Natalia
A1  - Shin, Jaeyoung
A1  - Werner, Isabella
A1  - Walther, Thomas
A1  - Schönburg, Markus
A1  - Pöling, Jochen
A1  - Warnecke, Henning
A1  - Braun, Thomas
A1  - Kostin, Sawa
A1  - Kubin, Thomas
T1  - Animal models and "omics" technologies for identification of novel biomarkers and drug targets to prevent heart failure
T2  - BioMed research international
N2  - It is now accepted that heart failure (HF) is a complex multifunctional disease rather than simply a hemodynamic dysfunction. Despite its complexity, stressed cardiomyocytes often follow conserved patterns of structural remodelling in order to adapt, survive, and regenerate. When cardiac adaptations cannot cope with mechanical, ischemic, and metabolic loads efficiently or become chronically activated, as, for example, after infection, then the ongoing structural remodelling and dedifferentiation often lead to compromised pump function and patient death. It is, therefore, of major importance to understand key events in the progression from a compensatory left ventricular (LV) systolic dysfunction to a decompensatory LV systolic dysfunction and HF. To achieve this, various animal models in combination with an “omics” toolbox can be used.  These approaches will ultimately lead to the identification of an arsenal of biomarkers and therapeutic targets which have the potential to shape the medicine of the future.
Y1  - 2015
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/39381
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-393810
SN  - 2314-6133
N1  - Copyright © 2015 Yunlong Hou et al. This is an open access article distributed under the   Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0/ , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
VL  - 2015
IS  - Article ID 212910
SP  - 1
EP  - 10
PB  - Hindawi
CY  - New York
ER  -