Abstract
Cardiac hypertrophy is a key biological response to injurious stresses such as pressure overload, and when excessive, leads to heart failure. Innate immune activation by danger signals, through intracellular pattern recognition receptors such as nucleotide-binding oligomerization domain-containing protein 1(Nod1) and its adaptor receptor-interacting protein 2 (RIP2) can play a major role in cardiac remodeling and progression to heart failure. We hypothesize that the danger signals originating from stressed mitochondria can be a major source modulator of innate immune activation, but the specific mechanism is to date unknown.
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