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Cardiac Fibrosis-Good, Bad or Dead
APS Cardiovascular Section
Suresh C. Tyagi
P.A. Lucchesi, F.J. Villarreal and J.S. Janicki
Cardiac fibrosis is manifested in many cardiac
abnormalities, and despite significant stride made toward the understanding
of mechanism of fibrosis, the molecular mechanism of development of cardiac
fibrosis, whether it is good, bad or dead, remains unclear. During fibrosis
and cardiac remodeling, inflammation and oxidative stress are elevated. The
role of inflammation, cytokines, growth factors and neurohumoral in
oxidative stress or vise versa is a controversial issue. It is clear,
however, that most of the silent and ubiquitous injury to a tissue is due,
in part, to oxyradicals generated by inflammatory and or mitochondrial NADPH
oxidase, masking the activity of superoxide dismutase and catalase.
Oxidative stress instigates decrease in endothelial nitric oxide (eNO), and
activates latent resident matrix metalloproteinase, as well as increases the
levels of cytokines, growth factors, and neurohormones. This starts a
vicious cycle of oxidative stress in which neurohormones such angiotensin II
increases further oxidative stress by decreasing the levels of bradykinin
and prostaglandins. This symposium will define the role of nitric oxide in
matrix remodeling and cardiac fibrosis by linking NO to remodeling,
structure and function.
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