ArticleJournal of immunology (Baltimore, Md. : 1950)2007
The anti-inflammatory effects of heat shock protein 72 involve inhibition of high-mobility-group box 1 release and proinflammatory function in macrophages.
Article in Journal of immunology (Baltimore, Md. : 1950), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 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
64 citing papers in PubMed, 127 citations in OpenAlex.
- Effects of heat stimulation after high-intensity interval training on serum adipokines, eHSP72, and immunoglobulins in men with obesity.Journal of exercise science and fitness · 2025Article
- HMGB1: A New Target for Ischemic Stroke and Hemorrhagic Transformation.Translational stroke research · 2025Review
- Important Role of Intestinal Microbiota in Chemotherapy-induced Diarrhea and Therapeutics.Journal of Cancer · 2025Review
- HMGB1 as an extracellular pro-inflammatory cytokine: Implications for drug-induced organic damage.Cell biology and toxicology · 2024Review
- Modulation of Abundance and Location of High-Mobility Group Box 1 in Human Microglia and Macrophages under Oxygen-Glucose Deprivation.ACS pharmacology & translational science · 2024Article
- Thermal Effect on Heat Shock Protein 70 Family to Prevent Atherosclerotic Cardiovascular Disease.Biomolecules · 2023Review
- Role of High Mobility Group Box 1 in Cardiovascular Diseases.Inflammation · 2022Review
- The mechanism of HMGB1 secretion and release.Experimental & molecular medicine · 2022Review
- Review: The role of HMGB1 in spinal cord injury.Frontiers in immunology · 2022Review
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- The performance of the alarmin HMGB1 in pediatric diseases: From lab to clinic.Immunity, inflammation and disease · 2021Review
- Damage-associated molecular patterns in trauma.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2020Review
- The effect of exposure time and concentration of airborne PMRedox biology · 2019Article
- HMGB1 protein as a novel target for cancer.Toxicology reports · 2019Review
- A longitudinal study of neurotrophic, oxidative, and inflammatory markers in first-onset depression in midlife women.European archives of psychiatry and clinical neuroscience · 2018Article
- ROS-induced HSP70 promotes cytoplasmic translocation of high-mobility group box 1b and stimulates antiviral autophagy in grass carp kidney cells.The Journal of biological chemistry · 2018Article
- Danger signals in trauma.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2018Review
- The Role of Danger Signals in the Pathogenesis and Perpetuation of Critical Illness.American journal of respiratory and critical care medicine · 2018Review
- Immune-Modulating Perspectives for Low Frequency Electromagnetic Fields in Innate Immunity.Frontiers in public health · 2018Review
4 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
6 authors at 4 institutions in 2 countries.
Funding
Abstract
High-mobility-group box 1 (HMGB1), a nuclear protein, has recently been identified as an important mediator of local and systemic inflammatory diseases when released into the extracellular milieu. Anti-inflammatory regulation by the stress response is an effective autoprotective mechanism when the host encounters harmful stimuli, but the mechanism of action remains incompletely delineated. In this study, we demonstrate that increases in levels of a major stress-inducible protein, heat shock protein 72 (Hsp72) by gene transfection attenuated LPS- or TNF-alpha-induced HMGB1 cytoplasmic translocation and release. The mechanisms involved inhibition of the chromosome region maintenance 1 (CRM1)-dependent nuclear export pathway. Overexpression of Hsp72 inhibited CRM1 translocation and interaction between HMGB1 and CRM1 in macrophages post-LPS and TNF-alpha treatment. In addition, overexpression of Hsp72 strongly inhibited HMGB1-induced cytokine (TNF-alpha, IL-1beta) expression and release, which correlated closely with: 1) inhibition of the MAP kinases (p38, JNK, and ERK); and 2) inhibition of the NF-kappaB pathway. Taken together, these experiments suggest that the anti-inflammatory activity of Hsp72 is achieved by interfering with both the release and proinflammatory function of HMGB1. Our experimental data provide important insights into the anti-inflammatory mechanisms of heat shock protein protection.
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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.