Mitochondrial ROS connects P2X7-mediated Ca2+ influx with IL-1α release by monocytes upon chronic tissue damage.

Whereas acute inflammation plays an important role in both tissue damage and repair, chronic inflammation favors tissue injury. Monocytes contribute to this deleterious effect by secreting proinflammatory cytokines. Amini et al. propose a novel mechanism involving adenosine triphosphate-induced purinergic P2X purinoceptor 7 receptor activation, which leads to calcium ion-dependent mitochondrial reactive oxygen species production, triggering interleukin-1α release by monocytes. This stimulates kidney immune cell infiltration and fibrosis in chronic kidney disease and promotes adverse cardiac remodeling following myocardial infarction.