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

doi:10.1016/j.jacbts.2019.01.008

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 journal › Article › Academic › peer-review

Abstract

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 language	English
Pages (from-to)	332-344
Number of pages	13
Journal	JACC: Basic to Translational Science
Volume	4
Issue number	3
DOIs	https://doi.org/10.1016/j.jacbts.2019.01.008
Publication status	Published - Jun 2019

Keywords

atrial cardiomyopathy
atrial fibrillation
ischemia/reperfusion
myocardial infarction
remote remodeling
CORONARY-ARTERY-DISEASE
HEART-FAILURE
MATRIX METALLOPROTEINASES
ISCHEMIC CARDIOMYOPATHY
VIABLE MYOCARDIUM
EMPTYING FUNCTION
FIBRILLATION
REVASCULARIZATION
MECHANISMS
INFARCTION

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Hohl, M., Erb, K., Lang, L., Ruf, S., Hübschle, T., Dhein, S., Linz, W., Elliott, A. D., Sanders, P., Zamyatkin, O., Böhm, M., Schotten, U., Sadowski, T., & Linz, D. (2019). Cathepsin A Mediates Ventricular Remote Remodeling and Atrial Cardiomyopathy in Rats With Ventricular Ischemia/Reperfusion. JACC: Basic to Translational Science, 4(3), 332-344. https://doi.org/10.1016/j.jacbts.2019.01.008

@article{483210d397724df8836587513e71e01e,

title = "Cathepsin A Mediates Ventricular Remote Remodeling and Atrial Cardiomyopathy in Rats With Ventricular Ischemia/Reperfusion",

abstract = "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.",

keywords = "atrial cardiomyopathy, atrial fibrillation, ischemia/reperfusion, myocardial infarction, remote remodeling, CORONARY-ARTERY-DISEASE, HEART-FAILURE, MATRIX METALLOPROTEINASES, ISCHEMIC CARDIOMYOPATHY, VIABLE MYOCARDIUM, EMPTYING FUNCTION, FIBRILLATION, REVASCULARIZATION, MECHANISMS, INFARCTION",

author = "Mathias Hohl and Katharina Erb and Lisa Lang and Sven Ruf and Thomas H{\"u}bschle and Stefan Dhein and Wolfgang Linz and Elliott, {Adrian D} and Prashanthan Sanders and Olesja Zamyatkin and Michael B{\"o}hm and Ulrich Schotten and Thorsten Sadowski and Dominik Linz",

note = "Publisher Copyright: {\textcopyright} 2019 The Authors",

year = "2019",

month = jun,

doi = "10.1016/j.jacbts.2019.01.008",

language = "English",

volume = "4",

pages = "332--344",

journal = "JACC: Basic to Translational Science",

issn = "2452-302X",

publisher = "Elsevier Inc.",

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Hohl, M, Erb, K, Lang, L, Ruf, S, Hübschle, T, Dhein, S, Linz, W, Elliott, AD, Sanders, P, Zamyatkin, O, Böhm, M, Schotten, U, Sadowski, T & Linz, D 2019, 'Cathepsin A Mediates Ventricular Remote Remodeling and Atrial Cardiomyopathy in Rats With Ventricular Ischemia/Reperfusion', JACC: Basic to Translational Science, vol. 4, no. 3, pp. 332-344. https://doi.org/10.1016/j.jacbts.2019.01.008

TY - JOUR

T1 - Cathepsin A Mediates Ventricular Remote Remodeling and Atrial Cardiomyopathy in Rats With Ventricular Ischemia/Reperfusion

AU - Hohl, Mathias

AU - Erb, Katharina

AU - Lang, Lisa

AU - Ruf, Sven

AU - Hübschle, Thomas

AU - Dhein, Stefan

AU - Linz, Wolfgang

AU - Elliott, Adrian D

AU - Sanders, Prashanthan

AU - Zamyatkin, Olesja

AU - Böhm, Michael

AU - Schotten, Ulrich

AU - Sadowski, Thorsten

AU - Linz, Dominik

PY - 2019/6

Y1 - 2019/6

N2 - 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.

AB - 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.

KW - atrial cardiomyopathy

KW - atrial fibrillation

KW - ischemia/reperfusion

KW - myocardial infarction

KW - remote remodeling

KW - CORONARY-ARTERY-DISEASE

KW - HEART-FAILURE

KW - MATRIX METALLOPROTEINASES

KW - ISCHEMIC CARDIOMYOPATHY

KW - VIABLE MYOCARDIUM

KW - EMPTYING FUNCTION

KW - FIBRILLATION

KW - REVASCULARIZATION

KW - MECHANISMS

KW - INFARCTION

U2 - 10.1016/j.jacbts.2019.01.008

DO - 10.1016/j.jacbts.2019.01.008

M3 - Article

C2 - 31312757

SN - 2452-302X

VL - 4

SP - 332

EP - 344

JO - JACC: Basic to Translational Science

JF - JACC: Basic to Translational Science

IS - 3

ER -

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

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Keywords

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