Figure 2.

Oxidative stress, immune response, inflammation, and apoptosis in cardiomyopathy. Endothelial dysfunction is a hallmark of cardiomyopathy. As in atherosclerotic plaques, mitochondrial dysfunction induces ROS to release. Thus, oxidative stress is due to a shift to more oxidative and less antioxidative factors. Again, the initial inflammatory response associated with increased oxidative stress consists of the infiltration of monocytes which differentiate to M1 macrophages secreting inflammatory cytokines. This inflammatory response also augments damage-associated molecular patterns (DAMPs), which trigger inflammation and mitochondrial ROS, inducing cell death. During the later phase of the immune response, T lymphocytes infiltrate. Cardiac T cells undergo a phenotypic change. Th2 and Treg cells decrease whereas Th1 and Th17 cells increase. This shift increases inflammatory cytokines and ROS, inducing cardiac apoptosis. Upregulated regulators are in yellow circles, downregulated ones in blue circles. Upregulated non-coding RNAs are in brown, down-regulated ones in blue.