ReviewShock (Augusta, Ga.)2009
Novel HMGB1-inhibiting therapeutic agents for experimental sepsis.
Review in Shock (Augusta, Ga.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.
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
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.
- Human recombinant protein C for severe sepsis and septic shock in adult and paediatric patients.The Cochrane database of systematic reviews · 2012Pooled it
- MEGF9 prevents lipopolysaccharide-induced cardiac dysfunction through activating AMPK pathway.Redox report : communications in free radical research · 2025Article
- Sepsis-Induced Cardiomyopathy and Cardiac Arrhythmias: Pathophysiology and Implications for Novel Therapeutic Approaches.Biomedicines · 2025Review
- sTREM-1, HMGB1, CRP, PCT, sCD14-ST, IL-6, IL-10, sHLA-G, and Vitamin D in Relation to Clinical Scores and Survival in SIRS/Sepsis.Biomedicines · 2025Article
- Toll like receptor 2 mediated exacerbation of sepsis associated acute kidney injury by renal congestion in mice.Scientific reports · 2025Article
- Septic Cardiomyopathy: Difficult Definition, Challenging Diagnosis, Unclear Treatment.Journal of clinical medicine · 2025Review
- Sepsis-induced cardiomyopathy: understanding pathophysiology and clinical implications.Archives of toxicology · 2025Review
- Mechanisms of mitochondrial damage-associated molecular patterns associated with inflammatory response in cardiovascular diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- The Interaction of HMGB1 with the Proinflammatory TREM-1 Receptor Generates Cytotoxic Lymphocytes Active against HLA-Negative Tumor Cells.International journal of molecular sciences · 2024Article
- Connexin 43 and Pannexin 1 hemichannels as endogenous regulators of innate immunity in sepsis.Frontiers in immunology · 2024Review
- The effects of etomidate on expression of high mobility group box 1 via the nuclear factor kappa B pathway in rat model of sepsis.The Libyan journal of medicine · 2023Article
- High mobility group box-1: a potential therapeutic target for allergic rhinitis.European journal of medical research · 2023Review
- Research progress in effects of pyroptosis on intestinal inflammatory injury.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023Article
- Review
- The SIRT1-HMGB1 axis: Therapeutic potential to ameliorate inflammatory responses and tumor occurrence.Frontiers in cell and developmental biology · 2022Review
- Septic cardiomyopathy: Diagnosis and management.Journal of intensive medicine · 2022Review
- Review
- MicroRNA-181b Inhibits Inflammatory Response and Reduces Myocardial Injury in Sepsis by Downregulating HMGB1.Inflammation · 2021Article
- LPS Primes Brain Responsiveness to High Mobility Group Box-1 Protein.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Pathophysiology of sepsis-induced cardiomyopathy.Nature reviews. Cardiology · 2021Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Sepsis refers to a systemic inflammatory response syndrome resulting from a microbial infection. The inflammatory response is partly mediated by innate immune cells (such as macrophages, monocytes, and neutrophils), which not only ingest and eliminate invading pathogens but also initiate an inflammatory response by producing early (e.g., TNF and IFN-gamma) and late (e.g., high-mobility group box [HMGB1]) proinflammatory cytokines. Here, we briefly review emerging evidence that support extracellular HMGB1 as a late mediator of experimental sepsis and discuss therapeutic potential of several HMGB1-inhibiting agents (including neutralizing antibodies and steroid-like tanshinones) in experimental sepsis.
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.