ReviewBiochemical pharmacology2008
Sepsis, apoptosis and complement.
Review in Biochemical pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 61 citations in OpenAlex.
- Crosstalk of regulated cell death pathways in sepsis-associated acute kidney injury: implications for therapy.Frontiers in cell and developmental biology · 2026Review
- Astragalus Polysaccharides Alleviate Sepsis by Boosting Adrenal Hormone Synthesis and Repairing Microvascular Damage.Applied biochemistry and biotechnology · 2025Article
- The Role of Mitochondrial Dysfunction and Inflammatory Response in the Pathogenesis of Sepsis-Induced Myocardial Injury: A Mechanistic Study.Journal of inflammation research · 2025Review
- Identification of immune-related lncRNA in sepsis by construction of ceRNA network and integrating bioinformatic analysis.BMC genomics · 2023Article
- Current insight on the mechanisms of programmed cell death in sepsis-induced myocardial dysfunction.Frontiers in cell and developmental biology · 2023Review
- Central role of microglia in sepsis-associated encephalopathy: From mechanism to therapy.Frontiers in immunology · 2022Review
- Left Ventricular Impaired Relaxation and Interstitial Myocarditis Identified in Sepsis-Associated Cardiac Dysfunction: Use of a Rodent Model.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Hemorrhagic shock induces renal complement activation.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2021Article
- Complement Inhibition and COVID-19: The Story so Far.ImmunoTargets and therapy · 2021Review
- Adenovirus-Extracellular Protein Interactions and Their Impact on Innate Immune Responses by Human Mononuclear Phagocytes.Viruses · 2020Review
- Complement as a Major Inducer of Harmful Events in Infectious Sepsis.Shock (Augusta, Ga.) · 2020Review
- Deciphering the Intricate Roles of Radiation Therapy and Complement Activation in Cancer.International journal of radiation oncology, biology, physics · 2020Review
- Treatment of Rare Inflammatory Kidney Diseases: Drugs Targeting the Terminal Complement Pathway.Frontiers in immunology · 2020Review
- High lncRNA MEG3 expression is associated with high mortality rates in patients with sepsis and increased lipopolysaccharide-induced renal epithelial cell and cardiomyocyte apoptosis.Experimental and therapeutic medicine · 2019Article
- G2A Protects Mice against Sepsis by Modulating Kupffer Cell Activation: Cooperativity with Adenosine Receptor 2b.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Neuroprotective effects of intravenous immunoglobulin are mediated through inhibition of complement activation and apoptosis in a rat model of sepsis.Intensive care medicine experimental · 2017Article
- Inhibition of miR-155 Protects Against LPS-induced Cardiac Dysfunction and Apoptosis in Mice.Molecular therapy. Nucleic acids · 2016Article
- C5a induces caspase-dependent apoptosis in brain vascular endothelial cells in experimental lupus.Immunology · 2016Article
- Identification of microRNA as sepsis biomarker based on miRNAs regulatory network analysis.BioMed research international · 2014Article
- Chlorogenic acid attenuates high mobility group box 1 (HMGB1) and enhances host defense mechanisms in murine sepsis.Molecular medicine (Cambridge, Mass.) · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Programmed cell death (apoptosis) is a prominent feature in human and experimental sepsis, especially as it involves the lymphoid system with resulting immunoparalysis. In addition, sepsis is associated with strong activation of the complement system, resulting in generation of the powerful anaphylatoxin, C5a, as well as the upregulation of the C5a receptor (C5aR) in a variety of different organs. The consequences of C5a interactions with C5aR can be directly linked to apoptosis of thymocytes and adrenal medullary cells after cecal ligation and puncture (CLP)-induced sepsis in rodents, as well as with other accompanying complications of CLP: cardiac dysfunction, consumptive coagulopathy, organ dysfunction, and lethality. This communication reviews the evidence for the adverse roles of C5a and C5aR in the setting of experimental sepsis and linkages to the various complications of sepsis, especially apoptosis as well as the roles of the two C5a receptors (C5aR and C5L2) in experimental sepsis.
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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.