Fig. 4

A schematic representation of MtDNA generation and diffusion and its role in CVD risk. Exposure to uremic milieu leads to redox imbalance and oxidative stress, which disrupts mitochondrial ultrastructure, causing the release of MtDNA into the cytosol and bloodstream. Free MtDNA molecules can be internalized by CMECs to elicit a sterile inflammatory response. This inflammatory challenge may subsequently lead to microvascular dysfunction and ultimately enhance CVD development