ArticlePharmaceuticals (Basel, Switzerland)2021
Matrix Metalloproteinase-2 Inhibition in Acute Ischemia-Reperfusion Heart Injury-Cardioprotective Properties of Carvedilol.
Article in Pharmaceuticals (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Myocardial Ischemia/Reperfusion Injury: Molecular Insights, Forensic Perspectives, and Therapeutic Horizons.Cells · 2025Review
- Matrix Metalloproteinases: Pathophysiologic Implications and Potential Therapeutic Targets in Cardiovascular Disease.Biomolecules · 2025Review
- Involvement of Oxidative Stress and Antioxidants in Modification of Cardiac Dysfunction Due to Ischemia-Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2025Review
- Nebivolol in oral subacute treatment prevents cardiac post-ischemic dysfunction in rats, but hyperthyroidism reduces this protection: mechanisms involved.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Matrix Metalloproteinases and Heart Transplantation-A Pathophysiological and Clinical View.Medicina (Kaunas, Lithuania) · 2023Review
- The β1 Adrenergic Blocker Nebivolol Ameliorates Development of Endotoxic Acute Lung Injury.Journal of clinical medicine · 2023Article
- Article
- Novel Roles of MT1-MMP and MMP-2: Beyond the Extracellular Milieu.International journal of molecular sciences · 2022Review
- Matrix Metalloproteinase 2 as a Pharmacological Target in Heart Failure.Pharmaceuticals (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Matrix metalloproteinase 2 (MMP-2) is activated in hearts upon ischemia-reperfusion (IR) injury and cleaves sarcomeric proteins. It was shown that carvedilol and nebivolol reduced the activity of different MMPs. Hence, we hypothesized that they could reduce MMPs activation in myocytes, and therefore, protect against cardiac contractile dysfunction related with IR injury. Isolated rat hearts were subjected to either control aerobic perfusion or IR injury: 25 min of aerobic perfusion, followed by 20 min global, no-flow ischemia, and reperfusion for 30 min. The effects of carvedilol, nebivolol, or metoprolol were evaluated in hearts subjected to IR injury. Cardiac mechanical function and MMP-2 activity in the heart homogenates and coronary effluent were assessed along with troponin I content in the former. Only carvedilol improved the recovery of mechanical function at the end of reperfusion compared to IR injury hearts. IR injury induced the activation and release of MMP-2 into the coronary effluent during reperfusion. MMP-2 activity in the coronary effluent increased in the IR injury group and this was prevented by carvedilol. Troponin I levels decreased by 73% in IR hearts and this was abolished by carvedilol. Conclusions: These data suggest that the cardioprotective effect of carvedilol in myocardial IR injury may be mediated by inhibiting MMP-2 activation.
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