ArticleJournal of the American Heart Association2014
Decreased myocardial injury and improved contractility after administration of a peptide derived against the alpha-interacting domain of the L-type calcium channel.
Article in Journal of the American Heart Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Novel Peptide Therapeutics Targeting the L-Type Calcium Channel Prevent Hypertrophic Cardiomyopathy by Decreasing Mitochondrial Energetics.JACC. Basic to translational science · 2025Article
- Impact of early myocardial injury on patients with severe pneumonia.Internal and emergency medicine · 2024Article
- Dynamic Changes in Ion Channels during Myocardial Infarction and Therapeutic Challenges.International journal of molecular sciences · 2024Review
- Peptides derived from high voltage-gated calcium channel β subunit reduce blood pressure in rats.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023Article
- Therapeutic Peptides to Treat Myocardial Ischemia-Reperfusion Injury.Frontiers in cardiovascular medicine · 2022Review
- Reactive oxygen species-based nanomaterials for the treatment of myocardial ischemia reperfusion injuries.Bioactive materials · 2022Review
- Hydroxysafflor Yellow A Ameliorates Myocardial Ischemia/Reperfusion Injury by Suppressing Calcium Overload and Apoptosis.Oxidative medicine and cellular longevity · 2021Article
- Characterization and validation of a preventative therapy for hypertrophic cardiomyopathy in a murine model of the disease.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Biochemical and toxicological effect of diazepam in stress-induced cardiac dysfunctions.Toxicology reports · 2020Article
- Partners in Crime: Towards New Ways of Targeting Calcium Channels.International journal of molecular sciences · 2019Review
- Dystrophic Cardiomyopathy-Potential Role of Calcium in Pathogenesis, Treatment and Novel Therapies.Genes · 2017Review
- Cardioprotection in ischaemia-reperfusion injury: novel mechanisms and clinical translation.The Journal of physiology · 2015Review
- Glutathionylation of the L-type Ca2+ channel in oxidative stress-induced pathology of the heart.International journal of molecular sciences · 2014Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMyocardial infarction remains the leading cause of morbidity and mortality associated with coronary artery disease. The L-type calcium channel (IC a-L) is critical to excitation and contraction. Activation of the channel also alters mitochondrial function. Here, we investigated whether application of a alpha-interacting domain/transactivator of transcription (AID-TAT) peptide, which immobilizes the auxiliary β2 subunit of the channel and decreases metabolic demand, could alter mitochondrial function and myocardial injury. METHODS AND
resultsTreatment with AID-TAT peptide decreased ischemia-reperfusion injury in guinea-pig hearts ex vivo (n=11) and in rats in vivo (n=9) assessed with uptake of nitroblue tetrazolium, release of creatine kinase, and lactate dehydrogenase. Contractility (assessed with catheterization of the left ventricle) was improved after application of AID-TAT peptide in hearts ex vivo (n=6) and in vivo (n=8) up to 12 weeks before sacrifice. In search of the mechanism for the effect, we found that intracellular calcium ([Ca(2+)]i, Fura-2), superoxide production (dihydroethidium fluorescence), mitochondrial membrane potential (Ψm, JC-1 fluorescence), reduced nicotinamide adenine dinucleotide production, and flavoprotein oxidation (autofluorescence) are decreased after application of AID-TAT peptide.
conclusionsApplication of AID-TAT peptide significantly decreased infarct size and supported contractility up to 12 weeks postcoronary artery occlusion as a result of a decrease in metabolic demand during reperfusion.
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Registered trials
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