Abstract
Heart failure (HF) is a cardiovascular syndrome characterized by maladaptive changes with an underlying inflammatory mediated pathogenesis. Nevertheless, current therapy is aimed at the heart workload and neurohormonal axis; thus, prognosis remains poor. To continue improving treatment, we rely on murine models for a better understanding of HF pathophysiology. Among them, pressure overload HF (PO-HF) animal models are a common strategy. Development of PO-HF is characterized by monocyte infiltration, which orchestrates a cascade of events leading to sustained inflammation and maladaptive changes. Here, we divide the PO-HF model progression into four phases and describe the inflammatory, structural, and gene expression profiles. This division is relevant due to its similarities with clinical hypertensive heart disease progression to HF. Evidence shows improvement in hemodynamic and other local parameters by altering the inflammatory response in a specific immune response at a specific point of time. Thus, it is relevant to focus on the time-dependent immune response interaction in order to provide more effective therapy. This review summarizes the pathogenesis of PO-HF murine models, highlighting the inflammatory events in a time frame view. By this approach, we expect to provide researchers with a better understanding of the intertwining time-dependent events that occur in PO-HF.
Highlights
Heart failure (HF) is a cardiovascular syndrome characterized by a structural and/or functional cardiac abnormality, resulting in reduced cardiac output and/or elevated intracardiac pressures [1]
The role of inflammation in HF was first described in 1990 by Levine et al, who established a correlation with the cytokine tumor necrosis factor α (TNFα), which was further evolved in the “Cytokine Hypothesis of Heart Failure” [10,11], in which a precipitating event could trigger elaboration of proinflammatory cytokines, accelerating the progression of HF [10,12]
The purpose of this review is to describe the pathogenesis of pressure overload HF (PO-HF) by highlighting the inflammatory events and their continuous changes in a novel and unique time frame view
Summary
Heart failure (HF) is a cardiovascular syndrome characterized by a structural and/or functional cardiac abnormality, resulting in reduced cardiac output and/or elevated intracardiac pressures [1]. Many aspects of its pathogenesis can be explained by the known biological effects of cytokines, and the pattern of expression of cytokines is related to the progression of HF [13,14,15] Following this line of thought and the limitations of the current therapy, there have been a variety of inflammatory mediators that researchers have attempted to use as therapeutic targets, among them TNFα and, more recently, interleukin(IL)-1β [13,16]. The former was targeted with the soluble TNF receptor, Etanercept [17], and TNFα monoclonal antibody, Infliximab [18], but results were not promising. We expect to provide researchers with a better understanding of the intertwining time-dependent events that occur in PO-HF
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