Oxidative Stress in Calcific Aortic Valve Stenosis: Protective Role of Natural Antioxidants

Figures

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  Figure 1. Illustrative diagram of the pathophysiology of CAVS. BMP—bone morphogenic protein, eNOS—endothelial Nitric oxide synthase, ICAM-1—intercellular adhesion molecule 1, IL—interleukin, NF-κB—nuclear factor κB, OPG—osteoprotegerin, Ox-LDLs—oxidized low-density lipoproteins, Ox-PLs—oxidized phospholipids, RANK—receptor activator of nuclear factor kappa B, RANKL—RANK ligand, ROS—reactive oxygen species, Runx2—runt-related transcription factor 2, TGF—transforming growth factor, TLRs—Toll-like receptors, VCAM-1—vascular cell adhesion protein 1, VICs—valvular interstitial cells, Wnt—wingless and Int, α-SMA—α-smooth muscle actin.

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  Figure 2. A diagram showing antioxidants with their mechanism of inhibition of CAVS. ROS is generated by different factors in cells, which can further activate various signaling pathways, leading to the release of transcription factors responsible for causing CAVS. Green rectangular boxes are antioxidants. The brown oval and the rectangular box indicate factors released during pathogenesis. The blue oval box represents signaling pathways. The red oval box indicates proteins. The pink text indicates proteins responsible for cellular differentiation. Red arrows indicate factors activated by ROS, and purple arrows indicate factors activating ROS. 10-DHGD—10 dehydrogingerdione, AKT —Protein Kinase B, ALP- Alkaline phosphatase, BMP—bone morphogenic protein, CAPE—Caffeic acid phenethyl ester, ERK—Extracellular signal-regulated kinase, IL—interleukin, NF-κB—nuclear factor κB, NLRP3—NLR family pyrin domain containing 3, ROS—reactive oxygen species, Runx2—runt-related transcription factor 2, SMAD—small mothers against decapentaplegic, TGF—Transforming Growth Factor, TLRs—Toll-like receptors, TNF—tumor necrosis factor, VICs—valvular interstitial cells, Wnt—wingless and Int.