Fig 5 Proposed mechanistic model linking dietary LA to cardiovascular disease pathogenesis.^{34 35 36 37 38 39 40 41 42 43 44 45 46 47 48} Conversion of LA to OXLAMs can proceed enzymatically, or via free radical mediated oxidative stress. Major sources of oxidative stress such as cigarette smoking and chronic alcohol exposure facilitate LA oxidation and production of oxidized low density lipoprotein (LDL). OXLAMs are the most abundant oxidized fatty acids in oxidized LDL and in atherosclerotic lesions. OXLAMs have been mechanistically linked to cardiovascular pathogenesis via multiple mechanisms. LDL=low density lipoprotein; CD36=cluster of differentiation 36 scavenger receptor; LOX 1=lectin like oxidized LDL receptor 1