Figure 3.

Systemic mitochondrial signaling may promote cardiovascular inflammation following anticancer therapy (CTx). CTx-induced cellular stress and death promote the release of damage-associated molecular patterns (DAMPs). DAMPs released from mitochondria include cell-free mitochondrial DNA (mtDNA), ATP, formyl peptides, and mitochondrial membrane fractions, among others. Circulating mitochondrial DAMPs are recognized by pattern recognition receptors of the innate immune system, including Toll-like receptors (TLRs), purinergic receptors, formyl peptide receptors (FPRs), and nucleotide-binding and oligomerization domain (NOD)-like receptors (NLRs). Activation of innate immune receptors on immune cells, cardiomyocytes, and vascular cells promotes cardiovascular inflammation that may play a role in CTx-induced cardiotoxicity. Image created with Biorender.com and published with permission.