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Redox à la carte: Novel chemogenetic models of heart failure
Ist Teil von
British journal of pharmacology, 2020-07, Vol.177 (14), p.3162-3167
Ort / Verlag
England: Blackwell Publishing Ltd
Erscheinungsjahr
2020
Link zum Volltext
Quelle
Wiley Online Library - AutoHoldings Journals
Beschreibungen/Notizen
Many current animal models of heart failure are hampered by intrinsic methodological complexities, while other models yield only a subtle cardiac phenotype even after prolonged in vivo treatments. A new ‘chemogenetic’ animal model of heart failure reproduces a critical characteristic shared by many disease states that lead to heart failure in humans: an increase in redox stress in the heart. This ‘chemogenetic’ approach exploits a recombinant yeast enzyme that can be dynamically and specifically activated in vivo to generate the ROS hydrogen peroxide (H2O2) in cardiac myocytes. Redox stress can be rapidly, selectively and reversibly manipulated by chemogenetic generation of ROS in cardiac myocytes, yielding a new model of dilated cardiomyopathy. Treatment of animals with the angiotensin receptor antagonist valsartan promotes recovery of ventricular function and resolution of adverse cardiac remodelling. This mini‐review discusses in vivo chemogenetic approaches to manipulate and analyse oxidative stress in the heart.