Cathepsin A Mediates Ventricular Remote Remodeling and Atrial Cardiomyopathy in Rats With Ventricular Ischemia/Reperfusion

Mathias Hohl, Katharina Erb, Lisa Lang, Sven Ruf, Thomas Hübschle, Stefan Dhein, Wolfgang Linz, Adrian D Elliott, Prashanthan Sanders, Olesja Zamyatkin, Michael Böhm, Ulrich Schotten, Thorsten Sadowski, Dominik Linz*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


After myocardial infarction, remote ventricular remodeling and atrial cardiomyopathy progress despite successful revascularization. In a rat model of ventricular ischemia/reperfusion, pharmacological inhibition of the protease activity of cathepsin A initiated at the time point of reperfusion prevented extracellular matrix remodeling in the atrium and the ventricle remote from the infarcted area. This scenario was associated with preservation of more viable ventricular myocardium and the prevention of an arrhythmogenic and functional substrate for atrial fibrillation. Remote ventricular extracellular matrix remodeling and atrial cardiomyopathy may represent a promising target for pharmacological atrial fibrillation upstream therapy following myocardial infarction.

Original languageEnglish
Pages (from-to)332-344
Number of pages13
JournalJACC: Basic to Translational Science
Issue number3
Publication statusPublished - Jun 2019

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