ArticleBasic research in cardiology2014
Ceramide-mediated depression in cardiomyocyte contractility through PKC activation and modulation of myofilament protein phosphorylation.
Article in Basic research in cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- Therapeutic potential of targeting ceramide for early cardiometabolic lipotoxicity in vivo study.Scientific reports · 2025Article
- Association of visceral adiposity index (VAI) with prognosis in patients with metabolic syndrome and heart failure with reduced ejection fraction.BMC cardiovascular disorders · 2025Article
- Sphingolipid Metabolism and Signalling Pathways in Heart Failure: From Molecular Mechanism to Therapeutic Potential.Journal of inflammation research · 2025Review
- Comparison and identification of serum metabolomic profiles in Stage B and Stage C ejection fraction preserved heart failure.Frontiers in cardiovascular medicine · 2025Article
- Magnetic resonance reveals early lipid deposition in murine prediabetes as predictive marker for cardiovascular injury.Npj imaging · 2024Article
- Diabetic cardiomyopathy: a brief summary on lipid toxicity.ESC heart failure · 2023Review
- Role of ceramides in diabetic foot ulcers (Review).International journal of molecular medicine · 2023Review
- Sphingolipid metabolism and signaling in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022Review
- Silencing ofInternational journal of molecular sciences · 2021Article
- Role of Ceramides in the Molecular Pathogenesis and Potential Therapeutic Strategies of Cardiometabolic Diseases: What we Know so Far.Frontiers in cell and developmental biology · 2021Review
- Measurement of Myofilament-Localized Calcium Dynamics in Adult Cardiomyocytes and the Effect of Hypertrophic Cardiomyopathy Mutations.Circulation research · 2019Article
- Getting to the heart of the sphingolipid riddle.Current opinion in physiology · 2018Article
- Adjustment of Dysregulated Ceramide Metabolism in a Murine Model of Sepsis-Induced Cardiac Dysfunction.International journal of molecular sciences · 2017Article
- Peroxisome proliferator-activated receptor-α expression induces alterations in cardiac myofilaments in a pressure-overload model of hypertrophy.American journal of physiology. Heart and circulatory physiology · 2017Article
- Chronic heart failure: Ca(2+), catabolism, and catastrophic cell death.Biochimica et biophysica acta · 2016Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Although ceramide accumulation in the heart is considered a major factor in promoting apoptosis and cardiac disorders, including heart failure, lipotoxicity and ischemia-reperfusion injury, little is known about ceramide's role in mediating changes in contractility. In the present study, we measured the functional consequences of acute exposure of isolated field-stimulated adult rat cardiomyocytes to C6-ceramide. Exogenous ceramide treatment depressed the peak amplitude and the maximal velocity of shortening without altering intracellular calcium levels or kinetics. The inactive ceramide analog C6-dihydroceramide had no effect on myocyte shortening or [Ca(2+)]i transients. Experiments testing a potential role for C6-ceramide-mediated effects on activation of protein kinase C (PKC) demonstrated evidence for signaling through the calcium-independent isoform, PKCε. We employed 2-dimensional electrophoresis and anti-phospho-peptide antibodies to test whether treatment of the cardiomyocytes with C6-ceramide altered myocyte shortening via PKC-dependent phosphorylation of myofilament proteins. Compared to controls, myocytes treated with ceramide exhibited increased phosphorylation of myosin binding protein-C (cMyBP-C), specifically at Ser273 and Ser302, and troponin I (cTnI) at sites apart from Ser23/24, which could be attenuated with PKC inhibition. We conclude that the altered myofilament response to calcium resulting from multiple sites of PKC-dependent phosphorylation contributes to contractile dysfunction that is associated with cardiac diseases in which elevations in ceramides are present.
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