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Redox à la carte: Novel chemogenetic models of heart failure
  • Andrea Sorrentino,
  • Thomas Michel
Andrea Sorrentino
Brigham and Women's Hospital Division of Cardiology

Corresponding Author:[email protected]

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Thomas Michel
Brigham and Women's Hospital
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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 recapitulates 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 reactive oxygen species (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 blocker valsartan promotes recovery of ventricular function and resolution of adverse cardiac remodeling. This Mini-Review discusses in vivo chemogenetic approaches to manipulate and analyze oxidative stress in the heart.
10 Feb 2020Submitted to British Journal of Pharmacology
12 Feb 2020Submission Checks Completed
12 Feb 2020Assigned to Editor
16 Feb 2020Reviewer(s) Assigned
21 Feb 2020Editorial Decision: Revise Minor
09 Mar 20201st Revision Received
10 Mar 2020Assigned to Editor
10 Mar 2020Submission Checks Completed
11 Mar 2020Reviewer(s) Assigned
12 Mar 2020Editorial Decision: Revise Minor
12 Mar 20202nd Revision Received
13 Mar 2020Assigned to Editor
13 Mar 2020Submission Checks Completed
15 Mar 2020Reviewer(s) Assigned
15 Mar 2020Editorial Decision: Accept