It is now accepted that heart failure (HF) is a complex multifunctional disease rather than simply a hemodynamic dysfunction.\nDespite its complexity, stressed cardiomyocytes often follow conserved patterns of structural remodelling in order to adapt, survive,\nand regenerate. When cardiac adaptations cannot cope with mechanical, ischemic, and metabolic loads efficiently or become\nchronically activated, as, for example, after infection, then the ongoing structural remodelling and dedifferentiation often lead\nto compromised pump function and patient death. It is, therefore, of major importance to understand key events in the progression\nfrom a compensatory left ventricular (LV) systolic dysfunction to a decompensatory LV systolic dysfunction and HF. To achieve\nthis, various animal models in combination with an ââ?¬Å?omicsââ?¬Â toolbox can be used. These approaches will ultimately lead to the\nidentification of an arsenal of biomarkers and therapeutic targets which have the potential to shape the medicine of the future.
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