ReviewCurrent pharmaceutical design2008
Sepsis: links between pathogen sensing and organ damage.
Review in Current pharmaceutical design, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 43 citations in OpenAlex.
- Boerhaave Syndrome-Narrative Review.Diagnostics (Basel, Switzerland) · 2025Review
- Host-Derived Cytotoxic Agents in Chronic Inflammation and Disease Progression.International journal of molecular sciences · 2023Review
- The implication of targeting PD-1:PD-L1 pathway in treating sepsis through immunostimulatory and anti-inflammatory pathways.Frontiers in immunology · 2023Review
- Sepsis triggered oxidative stress-inflammatory axis: the pathobiology of reprogramming in the normal sleep-wake cycle.Molecular and cellular biochemistry · 2022Review
- Article
- The Dual Role of Myeloperoxidase in Immune Response.International journal of molecular sciences · 2020Review
- Erastin Inhibits Septic Shock and Inflammatory Gene Expression via Suppression of the NF-κB Pathway.Journal of clinical medicine · 2019Article
- Deletion of Nlrp3 Augments Survival during Polymicrobial Sepsis by Decreasing Autophagy and Enhancing Phagocytosis.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Estrogen receptor α mediates the effects of notoginsenoside R1 on endotoxin-induced inflammatory and apoptotic responses in H9c2 cardiomyocytes.Molecular medicine reports · 2015Article
- Sepsis: Something old, something new, and a systems view.Journal of critical care · 2012Article
- Sepsis: from pattern to mechanism and back.Critical reviews in biomedical engineering · 2012Review
- Kukoamine B, a novel dual inhibitor of LPS and CpG DNA, is a potential candidate for sepsis treatment.British journal of pharmacology · 2011Article
- High-mobility group box-1 protein in tracheal aspirates from premature infants: relationship with bronchopulmonary dysplasia and steroid therapy.Journal of perinatology : official journal of the California Perinatal Association · 2010Article
- Differential regulation of the PGC family of genes in a mouse model of Staphylococcus aureus sepsis.PloS one · 2010Article
- Bench-to-bedside review: Glucose and stress conditions in the intensive care unit.Critical care (London, England) · 2010Review
- Zinc deficiency increases organ damage and mortality in a murine model of polymicrobial sepsis.Critical care medicine · 2009Article
- The role of the liver in sepsis.International reviews of immunologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The host's inflammatory response to sepsis can be divided into two phases, the initial detection and response to the pathogen initiated by the innate immune response, and the persistent inflammatory state characterized by multiple organ dysfunction syndrome (MODS). New therapies aimed at pathogen recognition receptors (PRRs) particularly the TLRs and the NOD-like receptors offer hope to suppress the initial inflammatory response in early sepsis and to bolster this response in late sepsis. The persistence of MODS after the initial inflammatory surge can also be a determining factor to host survival. MODS is due to the cellular damage and death induced by sepsis. The mechanism of this cell death depends in part upon mitochondrial dysfunction. Damaged mitochondria have increased membrane permeability prompting their autophagic removal if few mitochondria are involved but apoptotic cell death may occur if the mitochondrial losses are more extensive. In addition. severe loss of mitochondria results in low cell energy stores, necrotic cell death, and increased inflammation driven by the release of cell components such as HMGB1. Therapies, which aim at improving cellular energy reserves such as the promotion of mitochondrial biogenesis by insulin, may have a role in future sepsis therapies. Finally, both the inflammatory responses and the susceptibility to organ failure may be modulated by nutritional status and micronutrients, such as zinc, Therapies aimed at micronutrient repletion may further augment approaches targeting PRR function and mitochondrial viability.
Indexed as
Identifiers
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.