Inflame on!: mitochondrial escape provokes cytokine storms that doom the heart

Abstract

Mitochondria are derived from primordial bacterial endosymbionts and retain partial genomes. In mammalian cells, damaged or dysfunctional mitochondria are recognized, targeted for elimination, then neatly packaged and eliminated via mitophagy. A recent paper from Oka et al describes how interrupting normal mitophagic mitochondrial DNA degradation after pressure overload can activate Toll-like receptor-9 mediated innate immunity, causing myocardial inflammation that contributes to cardiomyopathic decompensation.