Figure 3
Physiological lipid handling is detailed in Figure 2 for comparison. PKC, protein kinase C; DAGs, diacylglycerols; Ca2+, calcium; PKG, protein kinase G; Nox2, nicotinamide adenine dinucleotide phosphate oxidase 2; NF-kB, nuclear factor kappa-light chain enhancer of activated B cells; MAPK, mitogen activated protein kinase; TGFb, transforming growth factor beta; O2−, superoxide anion radical.
Mechanisms by which lipid intermediates can promote the generation of reactive oxygen species (ROS), and by which ROS may go on to elicit diastolic dysfunction

Physiological lipid handling is detailed in Figure 2 for comparison. PKC, protein kinase C; DAGs, diacylglycerols; Ca2+, calcium; PKG, protein kinase G; Nox2, nicotinamide adenine dinucleotide phosphate oxidase 2; NF-kB, nuclear factor kappa-light chain enhancer of activated B cells; MAPK, mitogen activated protein kinase; TGFb, transforming growth factor beta; O2−, superoxide anion radical.

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