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

AF, atrial fibrillation CatA, cathepsin A Cx43, connexin 43 ECM, extracellular matrix I/R, ischemia/reperfusion ICM, ischemic cardiomyopathy LA, left atrial LAD, left anterior descending coronary artery LV, left ventricular MRI, magnetic resonance imaging PL, permanent left anterior descending ligation SAR, (S)-3-{[1-(2-Fluoro-phenyl)-5-methoxy-1H-pyrazole-3-carbonyl]-amino}-3-o-tolyl-propionic-acid atrial cardiomyopathy atrial fibrillation ischemia/reperfusion mRNA, messenger ribonucleic acid myocardial infarction remote remodeling

Journal

JACC. Basic to translational science
ISSN: 2452-302X
Titre abrégé: JACC Basic Transl Sci
Pays: United States
ID NLM: 101677259

Informations de publication

Date de publication:
Jun 2019
Historique:
received: 10 09 2018
revised: 08 01 2019
accepted: 11 01 2019
entrez: 18 7 2019
pubmed: 18 7 2019
medline: 18 7 2019
Statut: epublish

Résumé

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.

Identifiants

pubmed: 31312757
doi: 10.1016/j.jacbts.2019.01.008
pii: S2452-302X(19)30044-0
pmc: PMC6609908
doi:

Types de publication

Journal Article

Langues

eng

Pagination

332-344

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Auteurs

Mathias Hohl (M)

Klinik für Innere Medizin III, Universität des Saarlandes, Homburg/Saar, Germany.

Katharina Erb (K)

Klinik für Innere Medizin III, Universität des Saarlandes, Homburg/Saar, Germany.

Lisa Lang (L)

Klinik für Innere Medizin III, Universität des Saarlandes, Homburg/Saar, Germany.

Sven Ruf (S)

Sanofi-Aventis Deutschland GmbH, Frankfurt, Germany.

Thomas Hübschle (T)

Sanofi-Aventis Deutschland GmbH, Frankfurt, Germany.

Stefan Dhein (S)

Herzzentrum Leipzig Abt. Herzchirurgie, Leipzig, Germany.

Wolfgang Linz (W)

Sanofi-Aventis Deutschland GmbH, Frankfurt, Germany.

Adrian D Elliott (AD)

Centre for Heart Rhythm Disorders, South Australian Health and Medical Research Institute, Royal Adelaide Hospital, University of Adelaide, Adelaide, Australia.

Prashanthan Sanders (P)

Centre for Heart Rhythm Disorders, South Australian Health and Medical Research Institute, Royal Adelaide Hospital, University of Adelaide, Adelaide, Australia.

Olesja Zamyatkin (O)

Klinik für Innere Medizin III, Universität des Saarlandes, Homburg/Saar, Germany.

Michael Böhm (M)

Klinik für Innere Medizin III, Universität des Saarlandes, Homburg/Saar, Germany.

Ulrich Schotten (U)

Department of Physiology, University of Maastricht, Maastricht, the Netherlands.

Thorsten Sadowski (T)

Sanofi-Aventis Deutschland GmbH, Frankfurt, Germany.

Dominik Linz (D)

Klinik für Innere Medizin III, Universität des Saarlandes, Homburg/Saar, Germany.
Centre for Heart Rhythm Disorders, South Australian Health and Medical Research Institute, Royal Adelaide Hospital, University of Adelaide, Adelaide, Australia.

Classifications MeSH