Review Article
Postinfarct Left Ventricular Remodelling: A Prevailing Cause of Heart Failure
Table 1
Molecular pathways of ventricular remodelling. Many mediators have either an adaptive role (in bold) at low doses or a maladaptive role, with chronic/intense stimulation.
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JNK: Jun N-terminal kinase; ERK: extracellular-regulated kinase; JAK/STAT: Janus kinase/signal transducers and activators of transcription; ROS: reactive oxygen species; TNF-: tumor necrosis factor-; TRADD: TNF receptor-associated death domain; NF-κB: nuclear factor-κB; IGF-1: insulin-like growth factor-1; PDGF: platelet-derived growth factor; GDF-15: growth differentiation factor-15; HGF: hepatocyte growth factor; NRG-1: neuregulin-1; PI3K/AKT: phosphatidylinositol 3-kinase/AKT; NFAT: nuclear factor of activated T cells; PKA: protein kinase A; FAK: focal adhesion kinase. |