Nerve Kidney Macro vasculature
Figure 56.2 Biochemical pathways activating protein kinase C P (PKC p). AGE: advanced glycation end products; DAG: diacyl glycerol; PIP2: phosphoinositol diphosphate; IP3: inositol triphosphate.
stress and glycation process causes the activation of PKC to accelerate (Newton, 1995; Idris et al, 2001; Kawakami, 2002) (see Figure 56.2).
The principal isoforms that are activated are the P-and S-isoforms. Activation of PKC causes a number of pathological consequences, including alterations of endothelial nitric oxide synthase (eNOS), endothelin-1 (ET-1), vascular endothelial growth factor (VEGF), transforming TGF-P and PAI-1, as well as activation of NF-kB and NAD(P)H oxidases (Newton, 1995; Idris et al., 2001; Kawakami, 2002).
PKC activation, through phosphorylation of insulin receptor, causes resistance to insulin action. Since changes in insulin receptor signaling have been implicated in aging, the relevance of PKC changes to age-related increases in insulin resistance or to the aging process per se, remains speculative.
increased longevity, whereas PPAR S null mice have reduced life expectancy (Pardee et al., 2004). These observations highlight the central role of PPARs and FOXO in modulating the aging phenomenon.
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...