ArticleJournal of immunology (Baltimore, Md. : 1950)2016
Complement Destabilizes Cardiomyocyte Function In Vivo after Polymicrobial Sepsis and In Vitro.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 56 citations in OpenAlex.
- Extracellular Histones Associate with Blood-Brain Barrier Disruption and Astrocyte-Mediated Neuroinflammation During Polymicrobial Sepsis.International journal of molecular sciences · 2026Article
- Sepsis-Induced Cardiomyopathy and Cardiac Arrhythmias: Pathophysiology and Implications for Novel Therapeutic Approaches.Biomedicines · 2025Review
- Immunomodulatory and cardio-protective effects of differentially originated multipotent mesenchymal stroma cells during polymicrobial sepsis in mice.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2025Article
- The Impact of Extracellular Histones and Absence of Toll-like Receptors on Cardiac Functional and Electrical Disturbances in Mouse Hearts.International journal of molecular sciences · 2024Article
- Silenced-C5ar1 improved multiple organ injury in sepsis rats via inhibiting neutrophil extracellular trap.Journal of molecular histology · 2024Article
- C5aR2 Deficiency Lessens C5aR1 Distribution and Expression in Neutrophils and Macrophages.Journal of immunology research · 2024Article
- Inflammatory mechanisms and intervention strategies for sepsis-induced myocardial dysfunction.Immunity, inflammation and disease · 2023Review
- Sepsis: network pathophysiology and implications for early diagnosis.American journal of physiology. Regulatory, integrative and comparative physiology · 2023Review
- Research Progress on the Mechanism and Management of Septic Cardiomyopathy: A Comprehensive Review.Emergency medicine international · 2023Review
- Lipid oxidation dysregulation: an emerging player in the pathophysiology of sepsis.Frontiers in immunology · 2023Review
- TRPC channels blockade abolishes endotoxemic cardiac dysfunction by hampering intracellular inflammation and CaNature communications · 2022Article
- An integrated analysis ofCancer innovation · 2022Article
- Review
- Complement Activation in Patients With Heat-Related Illnesses: Soluble CD59 Is a Novel Biomarker Indicating Severity of Heat-Related Illnesses.Critical care explorations · 2022Article
- Cardiac alterations following experimental hip fracture - inflammaging as independent risk factor.Frontiers in immunology · 2022Article
- Complement as driver of systemic inflammation and organ failure in trauma, burn, and sepsis.Seminars in immunopathology · 2021Review
- Differential inflammatory responses of the native left and right ventricle associated with donor heart preservation.Physiological reports · 2021Article
- Systemic and local cardiac inflammation after experimental long bone fracture, traumatic brain injury and combined trauma in mice.Journal of orthopaedic translation · 2021Article
- Role of complement and potential of complement inhibitors in myasthenia gravis and neuromyelitis optica spectrum disorders: a brief review.Journal of neurology · 2021Review
- Trauma, a Matter of the Heart-Molecular Mechanism of Post-Traumatic Cardiac Dysfunction.International journal of molecular sciences · 2021Review
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
There is accumulating evidence during sepsis that cardiomyocyte (CM) homeostasis is compromised, resulting in cardiac dysfunction. An important role for complement in these outcomes is now demonstrated. Addition of C5a to electrically paced CMs caused prolonged elevations of intracellular Ca(2+) concentrations during diastole, together with the appearance of spontaneous Ca(2+) transients. In polymicrobial sepsis in mice, we found that three key homeostasis-regulating proteins in CMs were reduced: Na(+)/K(+)-ATPase, which is vital for effective action potentials in CMs, and two intracellular Ca(2+) concentration regulatory proteins, that is, sarcoplasmic/endoplasmic reticulum calcium ATPase 2 and the Na(+)/Ca(2+) exchanger. Sepsis caused reduced mRNA levels and reductions in protein concentrations in CMs for all three proteins. The absence of either C5a receptor mitigated sepsis-induced reductions in the three regulatory proteins. Absence of either C5a receptor (C5aR1 or C5aR2) diminished development of defective systolic and diastolic echocardiographic/Doppler parameters developing in the heart (cardiac output, left ventricular stroke volume, isovolumic relaxation, E' septal annulus, E/E' septal annulus, left ventricular diastolic volume). We also found in CMs from septic mice the presence of defective current densities for Ik1, l-type calcium channel, and Na(+)/Ca(2+) exchanger. These defects were accentuated in the copresence of C5a. These data suggest complement-related mechanisms responsible for development of cardiac dysfunction during sepsis.
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