ArticleMolecular and cellular biochemistry2012
Myocardial infarction in mice alters sarcomeric function via post-translational protein modification.
Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- Implications of S-glutathionylation of sarcomere proteins in cardiac disorders, therapies, and diagnosis.Frontiers in cardiovascular medicine · 2022Pooled it
- Mending the Achilles heels of titin in cardiac and musculoskeletal disease.Biophysical reviews · 2026Review
- Titin modulation and left ventricular remodelling in chronic primary mitral regurgitation.Frontiers in cardiovascular medicine · 2026Article
- Cardiomyocytes in Hypoxia: Cellular Responses and Implications for Cell-Based Cardiac Regenerative Therapies.Bioengineering (Basel, Switzerland) · 2025Review
- Reactive oxygen species in the pathogenesis of sarcopenia.Free radical biology & medicine · 2025Review
- Myocardial Infarction Suppresses Protein Synthesis and Causes Decoupling of Transcription and Translation.JACC. Basic to translational science · 2024Article
- Protein Quality Control at the Sarcomere: Titin Protection and Turnover and Implications for Disease Development.Frontiers in physiology · 2022Review
- Interventricular Differences of Signaling Pathways-Mediated Regulation of Cardiomyocyte Function in Response to High Oxidative Stress in the Post-Ischemic Failing Rat Heart.Antioxidants (Basel, Switzerland) · 2021Article
- Acidosis modifies effects of phosphorylated tropomyosin on the actin-myosin interaction in the myocardium.Journal of muscle research and cell motility · 2021Article
- Cardiac myosin super relaxation (SRX): a perspective on fundamental biology, human disease and therapeutics.Biology open · 2021Review
- Redox Regulation by Protein S-Glutathionylation: From Molecular Mechanisms to Implications in Health and Disease.International journal of molecular sciences · 2020Review
- S-glutathionylation, friend or foe in cardiovascular health and disease.Redox biology · 2020Review
- Implications of the complex biology and micro-environment of cardiac sarcomeres in the use of high affinity troponin antibodies as serum biomarkers for cardiac disorders.Journal of molecular and cellular cardiology · 2020Review
- Functional outcomes of structural peculiarities of striated muscle tropomyosin.Journal of muscle research and cell motility · 2020Review
- Posttranslational modifications of titin from cardiac muscle: how, where, and what for?The FEBS journal · 2019Review
- Troponin I modulation of cardiac performance: Plasticity in the survival switch.Archives of biochemistry and biophysics · 2019Review
- Estrogen but not testosterone preserves myofilament function from doxorubicin-induced cardiotoxicity by reducing oxidative modifications.American journal of physiology. Heart and circulatory physiology · 2019Article
- Redox regulation of protein nanomechanics in health and disease: Lessons from titin.Redox biology · 2019Review
- Effects of an Interchain Disulfide Bond on Tropomyosin Structure: A Molecular Dynamics Study.International journal of molecular sciences · 2018Article
- Unique methionine-aromatic interactions govern the calmodulin redox sensor.Biochemical and biophysical research communications · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Myocardial physiology in the aftermath of myocardial infarction (MI) before remodeling is an under-explored area of investigation. Here, we describe the effects of MI on the cardiac sarcomere with focus on the possible contributions of reactive oxygen species. We surgically induced MI in 6-7-month-old female CD1 mice by ligation of the left anterior descending coronary artery. Data were collected 3-4 days after MI or sham (SH) surgery. MI hearts demonstrated ventricular dilatation and systolic dysfunction upon echo cardiographic analysis. Sub-maximum Ca-activated tension in detergent-extracted fiber bundles from papillary muscles increased significantly in the preparations from MI hearts. Ca(2+) sensitivity increased after MI, whereas cooperativity of activation decreased. To assess myosin enzymatic integrity we measured splitting of Ca-ATP in myofibrillar preparations, which demonstrated a decline in Ca-ATPase activity of myofilament myosin. Biochemical analysis demonstrated post-translational modification of sarcomeric proteins. Phosphorylation of cardiac troponin I and myosin light chain 2 was reduced after MI in papillary samples, as measured using a phospho-specific stain. Tropomyosin was oxidized after MI, forming disulfide products detectable by diagonal non-reducing-reducing SDS-PAGE. Our analysis of myocardial protein oxidation post-MI also demonstrated increased S-glutathionylation. We functionally linked protein oxidation with sarcomere function by treating skinned fibers with the sulfhydryl reducing agent dithiothreitol, which reduced Ca(2+) sensitivity in MI, but not SH, samples. Our data indicate important structural and functional alterations to the cardiac sarcomere after MI, and the contribution of protein oxidation to this process.
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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.