Corruption of coronary collateral growth in metabolic syndrome: Role of oxidative stress

Figure 1 Compensatory mechanism of coronary collateral growth/arteriogenesis. A: A non-functioning collateral between parallel circuits in the absence of flow obstruction; B: Following proximal occlusion, there is a pressure drop across the pre-existing collateral stimulated by shear stress-driven redirection of flow; C: A complex intracellular signaling cascade involving various growth factors act in a coordinated manner to facilitate migration and proliferation of endothelial and smooth muscle cells (likely fibroblasts), leading to enlargement/ formation of arteries, arterioles and capillaries.

Figure 2 “Redox-window” hypothesis on coronary collateral growth. Existence of a critical “redox-window” is required; either reductive or oxidative stress will corrupt collateral growth and redox-dependent growth-factor signaling. The figure illustrates the principal measure in our system-collateral growth-as a function of the redox state in cells. The summary of this concept is best described as, in situations where there is reductive stress or oxidative stress, collateral growth is corrupted because of either too many neutral or oxidized thiol groups.