Long-Term caspase inhibition ameliorates apoptosis, reduces myocardial troponin-I cleavage, protects left ventricular function, and attenuates remodeling in rats with myocardial infarction
Open accessAbstract
Objectives This study was designed to evaluate whether in vivo caspase inhibition can prevent myocardial contractile protein degradation, improve myocardial function, and attenuate ventricular remodeling.Background Apoptosis is thought to play an important role in the development and progression of heart failure (HF) after a myocardial infarction (MI). However, it is not known whether inhibiting apoptosis can attenuate left ventricular (LV) remodeling and minimize systolic dysfunction.Method A 28-day infusion of caspase inhibitor (n = 12) or vehicle (n = 9) was administered to rats immediately after an anterior MI. In addition, five sham-operated rats given the caspase inhibitor were compared with 17 untreated sham-operated animals to study effects in non-MI rats. Left ventricular function, remodeling parameters, and hemodynamics were studied four weeks later. Myocardial caspase 3 activation and troponin-I contractile protein cleavage were studied in the non-infarct, remote LV myocardium using Western blots. Apoptosis was assessed using immunohistochemistry for activated caspase-positive cells as well as the TUNEL method. Collagen volume was estimated using morphometry.Results Caspase inhibition reduced myocardial caspase 3 activation. This was accompanied by less cleavage of troponin-I, an important component of the cardiac contractile apparatus, and fewer apoptotic cardiomyocytes. Furthermore, caspase inhibition reduced LV-weight-to-body-weight ratio, decreased myocardial interstitial collagen deposition, attenuated LV remodeling, and better preserved LV systolic function after MI.Conclusions Caspase inhibition, started soon after MI and continued for four weeks, preserves myocardial contractile proteins, reduces systolic dysfunction, and attenuates ventricular remodeling. These findings may have important therapeutic implications in post-MI HF.
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Inhibiting caspases can both reduce the occurrence of heart failure or slow its progression after MI as well as improve contractile function.
“Accordingly, inhibiting caspases can both reduce the occurrence of heart failure or slow its progression after MI (45, 131, 374, 383, 384) as well as improve contractile function (45).”
From Cardiac remodeling in obesity (2008) · cites this paper as [45]
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- Authors
- Chandrashekhar, Y., Sen, S., Anway, R., Shuros, A., & Anand, I.
- Affiliations
- University of Minnesota (US)
- Corresponding author
- Chandrashekhar, Y.
- ORCID
- Anand, Inder
- Venue
- Journal of the American College of Cardiology
- Publisher
- Elsevier BV
- Published
- 2004-01
- Volume
- 43
- Issue
- 2
- Pages
- 295-301
- ISSN
- 0735-1097 (ISSN-L)
- OpenAlex
- W2058977728
- Cited by
- 149
- References
- 35
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 3 · 2023: 4 · 2021: 5 · 2020: 3 · 2019: 2 · 2018: 5 · 2017: 1 · 2016: 4 · 2015: 5 · 2014: 5 · 2013: 8 · 2012: 4
- FWCI
- 12.61
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of the American College of Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- caspase inhibition, myocardial infarction, cardiomyocyte apoptosis, caspase-3, left ventricular remodeling, systolic dysfunction, heart failure, interstitial collagen deposition, cardioprotection
- MeSH terms
- Amino Acid Chloromethyl Ketones, Animals, Heart Failure, Hemodynamics, Male, Myocardial Infarction, Ventricular Function, Left, Rats, Sprague-Dawley, Apoptosis, Ventricular Dysfunction, Left, Troponin I, Caspases, Ventricular Remodeling, Rats, Caspase 3, Caspase Inhibitors
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