Table 2.

Summary of the pathological characteristics of athero-thrombosis and aneurysm and the relevance of angpts.

Stages of development	Histological feature	Pathological mechanisms	Relevance to angpts
Atherosclerosis
Initiation	Fatty streak	Endothelial injury, inflammation	Angpt 2 promotes while angpt 1 inhibits endothelial activation to a pro-inflammatory phenotype [37].
Progression	Plaque stability	Advanced atherosclerotic plaque	Upregulation of angpt 2 inhibits atherosclerosis development in low-density receptor deficient mice by promoting nitric oxide inhibition of LDL oxidation [60].
Complications	Plaque rupture	Angiogenesis	Mice vaccinated against Tie-2 demonstrated a more stable phenotype and an increase in collagen content [66]. Angpt 2 has been shown to activate Tie-2 and stably interact with STAT 5 to potentially promote neoangiogenesis in advanced atherosclerosis [37]. Angiogenesis has been associated with plaque rupture [75]. Angpt 2 is associated with increased MMP-2 levels and can potentially promote unstable plaques with high microvessel density (MVD) [69].
AAA
Initiation	Dilation	Elastin and collagen degradation, inflammation	Angpt 1 upregulates the expression of apelin which has been shown to reduce aortic diameter, and preserve aortic elastin and collagen. Angpt 1 promotes downregulation of adhesion molecules inhibits inflammatory cell infiltrate [62]. Angpt 2 promotes inflammation by favouring vascular leakage by disrupting cell–cell junctions [76].
Progression	Continued extracellular matrix destruction	Angiogenesis and factors important in initiation	Angpt 1 promotes angiogenesis by increasing EC proliferation and inhibiting EC apoptosis [77,78]. Angpt 2 can promote both EC survival and apoptosis depending on VEGF concentrations [17,79,80].
Rupture	Aortic medial and adventitia tear	Angiogenesis	Increased medial neovascularization and overexpression of proangiogenic cytokines have been reported at the aneurysm rupture edge [81].