- AutorIn
- Stephan R. Künzel Technische Universität Dresden, Dresden, Germany#German Red Cross Blood Donation Service North-East, Dresden, Germany
- Luise WinterTechnische Universität Dresden, Dresden, Germany
- Maximilian HoffmannTechnische Universität Dresden, Dresden, Germany
- Theresa A. Kant
- Jessica Thiel
- Romy Kronstein-Wiedemann
- Erik Klapproth
- Kristina Lorenz
- Ali El-Armouche
- Susanne Kämmerer
- Titel
- Investigation of mesalazine as an antifibrotic drug following myocardial infarction in male mice
- Zitierfähige Url:
- https://nbn-resolving.org/urn:nbn:de:bsz:14-qucosa2-952381
- Quellenangabe
- Physiological reports
Erscheinungsjahr: 2023
Jahrgang: 11
Heft: 17
E-ISSN: 2051-817X
Artikelnummer: e15809 - Erstveröffentlichung
- 2023
- Abstract (EN)
- Objectives: Myocardial infarction (MI) initiates a complex reparative response during which damaged cardiac muscle is replaced by connective tissue. While the initial repair is essential for survival, excessive fibrosis post-MI is a primary contributor to progressive cardiac dysfunction, and ultimately heart failure. Currently, there are no approved drugs for the prevention or the reversal of cardiac fibrosis. Therefore, we tested the therapeutic potential of repurposed mesalazine as a post-MI therapy, as distinct antifibrotic effects have recently been demonstrated. Methods: At 8 weeks of age, MI was induced in male C57BL/6J mice by LAD ligation. Mesalazine was administered orally at a dose of 100 μg/g body weight in drinking water. Fluid intake, weight development, and cardiac function were monitored for 28 days post intervention. Fibrosis parameters were assessed histologically and via qPCR. Results: Compared to controls, mesalazine treatment offered no survival benefit. However, no adverse effects on heart and kidney function and weight development were observed, either. While total cardiac fibrosis remained largely unaffected by mesalazine treatment, we found a distinct reduction of perivascular fibrosis alongside reduced cardiac collagen expression. Conclusions: Our findings warrant further studies on mesalazine as a potential add-on therapy post-MI, as perivascular fibrosis development was successfully prevented.
- Andere Ausgabe
- Link zum Artikel, der zuerst in der Zeitschrift „ Physiological reports” im Verlag Wiley erschienen ist.
DOI: 10.14814/phy2.15809 - Verweis
- Ergänzendes Material ist unter folgendem Link zu finden.
Link: https://physoc.onlinelibrary.wiley.com/doi/10.14814/phy2.15809#support-information-section - Freie Schlagwörter (EN)
- drug repurposing, fibrosis, mesalazine, myocardial infarction
- Klassifikation (DDC)
- 570
- 610
- Verlag
- Wiley, Weinheim
- Förder- / Projektangaben
- Deutsche Forschungsgemeinschaft (DFG)
GRK 2251: Immunologische und zellbasierte Strategien bei metabolischen Erkrankungen
ID: 288034826 - Deutsche Forschungsgemeinschaft (DFG)
TRR 205: Die Nebenniere: Zentrales Relais in Gesundheit und Krankheit
ID: 314061271 - Version / Begutachtungsstatus
- publizierte Version / Verlagsversion
- URN Qucosa
- urn:nbn:de:bsz:14-qucosa2-952381
- Veröffentlichungsdatum Qucosa
- 06.11.2025
- Dokumenttyp
- Artikel
- Sprache des Dokumentes
- Englisch
- Lizenz / Rechtehinweis
CC BY 4.0