Is targeting eNOS a key mechanistic insight of cardiovascular defensive potentials of statins?

@article{Balakumar2012IsTE,
  title={Is targeting eNOS a key mechanistic insight of cardiovascular defensive potentials of statins?},
  author={Pitchai Balakumar and Sonam Kathuria and Gaurav Taneja and Sanjeev Kalra and Nanjaian Mahadevan},
  journal={Journal of molecular and cellular cardiology},
  year={2012},
  volume={52 1},
  pages={
          83-92
        }
}
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TLDR
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Possible involvement of PPARγ-associated eNOS signaling activation in rosuvastatin-mediated prevention of nicotine-induced experimental vascular endothelial abnormalities
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TLDR
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TLDR
The present review discusses the recent finding that statins slow down the progression of these neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease.
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Statins have biphasic potential either to promote or inhibit angiogenesis, and there is increasing evidence that statins improve endothelial function through molecular mechanisms that mediate an increase in endothelium-derived nitric oxide.
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The lipid-lowering drugs, 3-hydroxy-3-methylgulutaryl-coenzyme A (HMG-CoA) reductase inhibitors or statins, are used in the prevention and treatment of cardiovascular diseases. Recent experimental
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The present review addressed the underlying principles pertaining to the modulatory role of statins on PPARs and suggested that statins have two major roles: a well‐established cholesterol‐lowering effect through inhibition of HMG‐CoA‐reductase and a newly explored PPAR‐activating property, which could mediate most of cardiovascular protective pleiotropic effects of statin including anti‐inflammatory, antioxidant and anti‐fibrotic properties.
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This study deals with the results of many experimental and clinical investigations and established the possibility of using different classes of drugs, including ACE inhibitors, Ca-antagonists, AT and endothelin receptor antagonists, direct activator of adenyl cyclase, statins, antioxidants, L-arginine, phosphodiesterase inhibitors, beta-blockers and organic nitrates.
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Inhibition of LOX-1 by statins may relate to upregulation of eNOS.
TLDR
Observations indicate that statins attenuate the effect of ox-LDL on eNOS expression, which provides a potential mechanism of beneficial effects of statins beyond lowering cholesterol.
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