ReviewMolecular immunology2017
Complement and sepsis-induced heart dysfunction.
Review in Molecular immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 50 citations in OpenAlex.
- Protective role of selenium in sepsis: Mechanisms and potential therapeutic strategies.Open medicine (Warsaw, Poland) · 2025Review
- Brevilin A ameliorates sepsis-induced cardiomyopathy through inhibiting NLRP3 inflammation.Annals of medicine and surgery (2012) · 2023Article
- Article
- Myo-inositol oxygenase (MIOX) accelerated inflammation in the model of infection-induced cardiac dysfunction by NLRP3 inflammasome.Immunity, inflammation and disease · 2023Article
- Inflammatory mechanisms and intervention strategies for sepsis-induced myocardial dysfunction.Immunity, inflammation and disease · 2023Review
- Parecoxib attenuates inflammation injury in septic H9c2 cells by regulating the MAPK signaling pathway.Experimental and therapeutic medicine · 2023Article
- Hydrogen sulfide alleviates lipopolysaccharide-induced myocardial injury through TLR4-NLRP3 pathway.Physiological research · 2023Article
- The protective effect of the mitochondrial-derived peptide MOTS-c on LPS-induced septic cardiomyopathy.Acta biochimica et biophysica Sinica · 2023Article
- Cardioprotective Effects of Octreotide against Sepsis-Induced Cardiotoxicity in Mice.Archives of Razi Institute · 2023Article
- Lipid oxidation dysregulation: an emerging player in the pathophysiology of sepsis.Frontiers in immunology · 2023Review
- Protective effect of growth differentiation factor 15 in sepsis by regulating macrophage polarization and its mechanism.Bioengineered · 2022Article
- Binding of raloxifene to human complement fragment 5a (Journal of biomolecular structure & dynamics · 2022Article
- CD63 and C3AR1: The Potential Molecular Targets in the Progression of Septic Shock.International journal of general medicine · 2022Article
- Effects of extracellular histones on left ventricular diastolic function and potential mechanisms in mice with sepsis.American journal of translational research · 2022Article
- microRNA-193-3p attenuates myocardial injury of mice with sepsis via STAT3/HMGB1 axis.Journal of translational medicine · 2021Article
- Differential inflammatory responses of the native left and right ventricle associated with donor heart preservation.Physiological reports · 2021Article
- Inhibition of XBP1 Alleviates LPS-Induced Cardiomyocytes Injury by Upregulating XIAP through Suppressing the NF-κB Signaling Pathway.Inflammation · 2021Article
- Trauma, a Matter of the Heart-Molecular Mechanism of Post-Traumatic Cardiac Dysfunction.International journal of molecular sciences · 2021Review
- Complement as a Major Inducer of Harmful Events in Infectious Sepsis.Shock (Augusta, Ga.) · 2020Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
It is well known that cardiac dysfunction develops during sepsis in both humans and in rodents (rats, mice). These defects appear to be reversible, since after "recovery" from sepsis, cardiac dysfunction disappears and the heart returns to its function that was present before the onset of sepsis. Our studies, using in vivo and in vitro models, have demonstrated that C5a and its receptors (C5aR1 and C5aR2) play key roles in cardiac dysfunction developing during sepsis. Use of a neutralizing antibody to C5a largely attenuates cardiac dysfunction and other adverse events developing during sepsis. The molecular basis for cardiac dysfunctions is linked to generation of C5a and its interaction with C5a receptors present on surfaces of cardiomyocytes (CMs). It is established that C5a interactions with C5a receptors leads to significant reductions involving faulty contractility and relaxation in CMs. In addition, C5a interactions with C5a receptors on CMs results in reductions in Na
Indexed as
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What OpenQuestion holds
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.