Peripheral artery disease, redox signaling, oxidative stress - Basic and clinical aspects.
Journal article

Peripheral artery disease, redox signaling, oxidative stress - Basic and clinical aspects.

  • Steven S Laboratory of Molecular Cardiology, Center of Cardiology, Cardiology 1, Medical Center of the Johannes Gutenberg University, Mainz, Germany.
  • Daiber A Laboratory of Molecular Cardiology, Center of Cardiology, Cardiology 1, Medical Center of the Johannes Gutenberg University, Mainz, Germany. Electronic address: daiber@uni-mainz.de.
  • Dopheide JF Angiology, Center of Cardiology, Cardiology 1, Medical Center of the Johannes Gutenberg University, Mainz, Germany; Swiss Cardiovascular Center, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
  • Münzel T Laboratory of Molecular Cardiology, Center of Cardiology, Cardiology 1, Medical Center of the Johannes Gutenberg University, Mainz, Germany.
  • Espinola-Klein C Angiology, Center of Cardiology, Cardiology 1, Medical Center of the Johannes Gutenberg University, Mainz, Germany. Electronic address: espinola@uni-mainz.de.
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  • 2017-04-25
Published in:
  • Redox biology. - 2017
English Reactive oxygen and nitrogen species (ROS and RNS, e.g. H2O2, nitric oxide) confer redox regulation of essential cellular signaling pathways such as cell differentiation, proliferation, migration and apoptosis. At higher concentrations, ROS and RNS lead to oxidative stress and oxidative damage of biomolecules (e.g. via formation of peroxynitrite, fenton chemistry). Peripheral artery disease (PAD) is characterized by severe ischemic conditions in the periphery leading to intermittent claudication and critical limb ischemia (end stage). It is well known that redox biology and oxidative stress play an important role in this setting. We here discuss the major pathways of oxidative stress and redox signaling underlying the disease progression with special emphasis on the contribution of inflammatory processes. We also highlight therapeutic strategies comprising pharmacological (e.g. statins, angiotensin-converting enzyme inhibitors, phosphodiesterase inhibition) and non-pharmacological (e.g. exercise) interventions. Both of these strategies induce potent indirect antioxidant and anti-inflammatory mechanisms that may contribute to an improvement of PAD associated complications and disease progression by removing excess formation of ROS and RNS (e.g. by ameliorating primary complications such as hyperlipidemia and hypertension) as well as the normalization of the inflammatory phenotype suppressing the progression of atherosclerosis.
Language
  • English
Open access status
gold
Identifiers
Persistent URL
https://folia.unifr.ch/global/documents/278498
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