Aortic valve stenosis (AVS), a valvulopathy that threatens life quality and longevity, in particular in an aging population. Yet no medical treatment is to date available emphasizing the need for more mechanistic insight into the disease to provide future treatment targets. Obesity and genetic variants within genes involved in lipid metabolisms and lipoprotein (a) have emerged as risk factors for AVS as these variants have significant genome-wide associations. The metamorphosis of the aortic valve to severe calcification involves lipid infiltration, inflammation, and oxidative stress which promotes further calcification in a viscous cycle in tandem with biomechanical factors that trigger further recruitment of inflammatory cells. The resolution of inflammation is an active and regulated process which therefore offers new possible targets. Fatty acids serve as substrate for many lipid mediators involved in the resolution of inflammation which may counterbalance the inflammation by promoting macrophage-mediated healing leading to a dampened inflammatory response. Recent data have put fatty acids in the spotlight as an important mechanism in the development of aortic valve disease. This review discusses possible mechanisms exerted by fatty acids in the context of AVS to facilitate future search for therapeutic targets.
Keywords: calcification; inflammation; lipid mediators; valvular heart disease.