IL6 and cardiac hypertrophy: The myocyte-derived HSP90 orchestrates not only p65-mediated IL-6 synthesis but also its release in exosomal vesicles, and such exosomes and myocyte-secreted IL-6 are responsible in unison for the biphasic activation of STAT-3 signaling in cardiac fibroblasts that culminates in excess collagen synthesis, leading to severely compromised cardiac function during cardiac hypertrophy [24].