Figure 2.

MPs are involved in DN pathogenesis. With demonstrable increases in DN-related pathological contexts, MPs might be involved in DN via the mechanisms, including (1) Mediating transcellular crosstalk mainly by (a) delivering their content to recipient cells and releasing these bioactive substances or (b) binding to the target cell receptors via surface molecules (namely, receptor-ligand interaction); (2) Promoting partial or systemic IR, possibly by influencing the insulin-related Akt/PI3K signalling and blocking glucose uptake by hindering glucose transporter (GLUT); (3) Increasing the production of cytosolic ROS, which activates organelle oxidative stress of mitochondria and ER and triggers inflammatory responses; (4) Exerting functions associated with angiogenesis and apoptosis and communicating between podocytes and glomerular endothelial cells via the VEGF-A/VEGFR-2 system.