ArticleJournal of molecular and cellular cardiology2008
Calpain inhibition attenuates right ventricular contractile dysfunction after acute pressure overload.
Article in Journal of molecular and cellular cardiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Pterostilbene Reduces Experimental Myocardial Infarction-Induced Oxidative Stress in Lung and Right Ventricle.Arquivos brasileiros de cardiologia · 2022Article
- Spatio-temporal regulation of calpain activity after experimental myocardial infarction in vivo.Biochemistry and biophysics reports · 2021Article
- Nuclear localization of a novel calpain-2 mediated junctophilin-2 C-terminal cleavage peptide promotes cardiomyocyte remodeling.Basic research in cardiology · 2020Article
- Cardiac Protective Role of Heat Shock Protein 27 in the Stress Induced by Drugs of Abuse.International journal of molecular sciences · 2020Review
- Metabolic stress-induced cardiomyopathy is caused by mitochondrial dysfunction due to attenuated Erk5 signaling.Nature communications · 2017Article
- Early dystrophin loss is coincident with the transition of compensated cardiac hypertrophy to heart failure.PloS one · 2017Article
- Molecular Determinants of Calpain-dependent Cleavage of Junctophilin-2 Protein in Cardiomyocytes.The Journal of biological chemistry · 2015Article
- Calpain-dependent cleavage of junctophilin-2 and T-tubule remodeling in a mouse model of reversible heart failure.Journal of the American Heart Association · 2014Article
- The NO/ONOO-cycle as the central cause of heart failure.International journal of molecular sciences · 2013Review
- Regulation and physiological roles of the calpain system in muscular disorders.Cardiovascular research · 2012Review
- Calpain inhibition preserves talin and attenuates right heart failure in acute pulmonary hypertension.American journal of respiratory cell and molecular biology · 2012Article
- Calpain protects the heart from hemodynamic stress.The Journal of biological chemistry · 2011Article
- Tear me down: role of calpain in the development of cardiac ventricular hypertrophy.Circulation research · 2011Review
- Evaluation of right ventricular function.Current cardiology reports · 2011Review
- Myocardial function after fetal cardiac bypass in an ovine model.The Journal of thoracic and cardiovascular surgery · 2011Article
- In vivo administration of calpeptin attenuates calpain activation and cardiomyocyte loss in pressure-overloaded feline myocardium.American journal of physiology. Heart and circulatory physiology · 2008Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Right ventricular contractile failure from acute RV pressure overload is an important cause of morbidity and mortality, but the mechanism of RV failure in this setting is incompletely defined. We hypothesized that RV dysfunction from acute RV pressure overload is, in part, due to activation of calpain, and that calpain inhibition would therefore attenuate RV dysfunction. Anesthetized, open chest pigs were treated with the calpain inhibitor MDL-28170 or with inactive vehicle, and then subjected to acute RV pressure overload for 90 min. RV contractile function was assessed by the regional Frank-Starling relation. RV myocardial tissue was analyzed for evidence of calpain activation and calpain-mediated proteolysis. RV pressure overload caused severe contractile dysfunction, along with significant alterations in the endogenous calpain inhibitor calpastatin typical of calpain activation. MDL-28170 attenuated RV free wall dysfunction by more than 50%. However, there were no differences in degradation of spectrin, desmin, troponin-I or SERCA2 between SHAM operated pigs and pigs subjected to acute RV pressure overload, or between vehicle and MDL-28170 treated pigs. Acute RV pressure overload causes calpain activation, and RV contractile dysfunction from acute RV pressure overload is attenuated by the calpain inhibitor MDL-28170; however, the effect is not explained by inhibition of calpain-mediated degradation of spectrin, desmin, troponin-I or SERCA2. Because this is the first report of any agent that can directly attenuate RV contractile dysfunction in acute RV pressure overload, further investigation of the mechanism of action of MDL-28170 in this setting is warranted.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.