Figure legends
Figure 1 :
The pivotal role of ROS in endothelial dysfunction and CM
hypertrophy :
In patients with diabetes, hyperglycaemia along with inflammatory
reaction, enhanced cyclic stretch and oscillatory shear stress,
increases production of reactive oxygen species in endothelial cells
(ECs). ROS trigger vascular inflammation via activating multiple
downstream pathways, including extracellular signal-regulating kinase
(ERK), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein
kinase (p38 MAPK), as well by increasing the expression of nuclear
factor kappa B (NF-κB). Excessive ROS induce uncoupling of endothelial
nitric oxide synthase (eNOS) and loss of nitric oxide (NO)
bioavailability of endothelial cells. The latter results in the
inactivation of protein kinase G-cyclic guanosine monophosphate
(PKG-cGMP) and hypo-phosphorylation of titin in adjacent cardiomyocyte
(CM), therefore promoting CM hypertrophy. Increased ROS production
promotes the formation of F-actin stress fibre and vascular endothelial
(VE)-caherin internalisation via activing src family kinase (SFK),
leading to the disruption of adherens junction (Created with
Biorender.com).