ArticleAmerican journal of physiology. Heart and circulatory physiology2013
SERCA Cys674 sulphonylation and inhibition of L-type Ca2+ influx contribute to cardiac dysfunction in endotoxemic mice, independent of cGMP synthesis.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- HDAC1-mediated SUCLA2 lysine β-hydroxybutyrylation modulates myocardial mitochondrial function in sepsis-induced heart dysfunction.Redox biology · 2026Article
- Mitochondria at the Heart of Sepsis: Mechanisms, Metabolism, and Sex Differences.International journal of molecular sciences · 2025Review
- Oxidative stress and atrial fibrillation.Journal of molecular and cellular cardiology · 2024Review
- Article
- Vericiguat suppresses ventricular tachyarrhythmias inducibility in a rabbit myocardial infarction model.PloS one · 2024Article
- NADPH Oxidases and Oxidative Stress in the Pathogenesis of Atrial Fibrillation.Antioxidants (Basel, Switzerland) · 2023Review
- Gut Molecules in Cardiometabolic Diseases: The Mechanisms behind the Story.International journal of molecular sciences · 2023Review
- Editorial: The role of calcium and calcium binding proteins in cell physiology and disease.Frontiers in physiology · 2023Article
- TRPC channels blockade abolishes endotoxemic cardiac dysfunction by hampering intracellular inflammation and CaNature communications · 2022Article
- Mitochondria-endoplasmic reticulum contacts in sepsis-induced myocardial dysfunction.Frontiers in cell and developmental biology · 2022Review
- ER stress and calcium-dependent arrhythmias.Frontiers in physiology · 2022Review
- PKCδ causes sepsis-induced cardiomyopathy by inducing mitochondrial dysfunction.American journal of physiology. Heart and circulatory physiology · 2020Article
- The Control of Diastolic Calcium in the Heart: Basic Mechanisms and Functional Implications.Circulation research · 2020Review
- Toll-Like Receptor-Mediated Cardiac Injury during Experimental Sepsis.Mediators of inflammation · 2020Article
- Mitochondrial and Sarcoplasmic Reticulum Interconnection in Cardiac Arrhythmia.Frontiers in cell and developmental biology · 2020Review
- Effect of landiolol on sex-related transcriptomic changes in the myocardium during sepsis.Intensive care medicine experimental · 2019Article
- HAX-1 regulates SERCA2a oxidation and degradation.Journal of molecular and cellular cardiology · 2018Article
- Complement and sepsis-induced heart dysfunction.Molecular immunology · 2017Review
- Distinct Myocardial Mechanisms Underlie Cardiac Dysfunction in Endotoxemic Male and Female Mice.Shock (Augusta, Ga.) · 2016Article
- The synthetic antimicrobial peptide 19-2.5 attenuates septic cardiomyopathy and prevents down-regulation of SERCA2 in polymicrobial sepsis.Scientific reports · 2016Article
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
The goal of this study was to identify the cellular mechanisms responsible for cardiac dysfunction in endotoxemic mice. We aimed to differentiate the roles of cGMP [produced by soluble guanylyl cyclase (sGC)] versus oxidative posttranslational modifications of Ca(2+) transporters. C57BL/6 mice [wild-type (WT) mice] were administered lipopolysaccharide (LPS; 25 μg/g ip) and euthanized 12 h later. Cardiomyocyte sarcomere shortening and Ca(2+) transients (ΔCai) were depressed in LPS-challenged mice versus baseline. The time constant of Ca(2+) decay (τCa) was prolonged, and sarcoplasmic reticulum Ca(2+) load (CaSR) was depressed in LPS-challenged mice (vs. baseline), indicating decreased activity of sarco(endo)plasmic Ca(2+)-ATPase (SERCA). L-type Ca(2+) channel current (ICa,L) was also decreased after LPS challenge, whereas Na(+)/Ca(2+) exchange activity, ryanodine receptors leak flux, or myofilament sensitivity for Ca(2+) were unchanged. All Ca(2+)-handling abnormalities induced by LPS (the decrease in sarcomere shortening, ΔCai, CaSR, ICa,L, and τCa prolongation) were more pronounced in mice deficient in the sGC main isoform (sGCα1(-/-) mice) versus WT mice. LPS did not alter the protein expression of SERCA and phospholamban in either genotype. After LPS, phospholamban phosphorylation at Ser(16) and Thr(17) was unchanged in WT mice and was increased in sGCα1(-/-) mice. LPS caused sulphonylation of SERCA Cys(674) (as measured immunohistochemically and supported by iodoacetamide labeling), which was greater in sGCα1(-/-) versus WT mice. Taken together, these results suggest that cardiac Ca(2+) dysregulation in endotoxemic mice is mediated by a decrease in L-type Ca(2+) channel function and oxidative posttranslational modifications of SERCA Cys(674), with the latter (at least) being opposed by sGC-released cGMP.
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