ArticleJournal of immunology (Baltimore, Md. : 1950)2007
Nuclear heat shock protein 72 as a negative regulator of oxidative stress (hydrogen peroxide)-induced HMGB1 cytoplasmic translocation and release.
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 57 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
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.
- Concentrations of HMGB1 and Hsp70 of healthy subjects in upper and lower airway: Literature Review and Meta-analysis.International journal of medical sciences · 2021Pooled it
- Trial
- Complementary roles of HMGB1 and PRDX4 in the pathophysiology of steroid-associated osteonecrosis of the femoral head: a histopathological and immunohistochemistry study.Virchows Archiv : an international journal of pathology · 2026Article
- Natural compounds and programmed necrosis: pioneering a new frontier in cancer treatments.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Targeting the MCP-GPX4/HMGB1 Axis for Effectively Triggering Immunogenic Ferroptosis in Pancreatic Ductal Adenocarcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- 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
- Flavonoids Regulate Redox-Responsive Transcription Factors in Glioblastoma and Microglia.Cells · 2023Article
- Never in mitosis gene A-related kinase-6 deficiency deteriorates diabetic cardiomyopathy via regulating heat shock protein 72.Journal of molecular medicine (Berlin, Germany) · 2023Article
- Secretory autophagy machinery and vesicular trafficking are involved in HMGB1 secretion.Autophagy · 2021Article
- Review
- Article
- Airway epithelial ITGB4 deficiency in early life mediates pulmonary spontaneous inflammation and enhanced allergic immune response.Journal of cellular and molecular medicine · 2020Article
- A proteome-wide assessment of the oxidative stress paradigm for metal and metal-oxide nanomaterials in human macrophages.NanoImpact · 2020Article
- Role of 72-kDa Heat Shock Protein in Heat-stimulated Regeneration of Injured Muscle in Rat.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019Article
- Targeting epigenetic mechanisms in diabetic wound healing.Translational research : the journal of laboratory and clinical medicine · 2019Review
- Phosphorylation of nuclear Tau is modulated by distinct cellular pathways.Scientific reports · 2018Article
- HMGB1 deficiency reduces HJournal of cellular and molecular medicine · 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
- The Role of Danger Signals in the Pathogenesis and Perpetuation of Critical Illness.American journal of respiratory and critical care medicine · 2018Review
- Regulation of Tumor Progression by Programmed Necrosis.Oxidative medicine and cellular longevity · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
In response to inflammatory stimuli (e.g., endotoxin, proinflammatory cytokines) or oxidative stress, macrophages actively release a ubiquitous nuclear protein, high-mobility group box 1 (HMGB1), to sustain an inflammatory response to infection or injury. In this study, we demonstrated mild heat shock (e.g., 42.5 degrees C, 1 h), or enhanced expression of heat shock protein (Hsp) 72 (by gene transfection) similarly rendered macrophages resistant to oxidative stress-induced HMGB1 cytoplasmic translocation and release. In response to oxidative stress, cytoplasmic Hsp72 translocated to the nucleus, where it interacted with nuclear proteins including HMGB1. Genetic deletion of the nuclear localization sequence (NLS) or the peptide binding domain (PBD) from Hsp72 abolished oxidative stress-induced nuclear translocation of Hsp72-DeltaNLS (but not Hsp72-DeltaPBD), and prevented oxidative stress-induced Hsp72-DeltaPBD-HMGB1 interaction in the nucleus. Furthermore, impairment of Hsp72-DeltaNLS nuclear translocation, or Hsp72-DeltaPBD-HMGB1 interaction in the nucleus, abrogated Hsp72-mediated suppression of HMGB1 cytoplasmic translocation and release. Taken together, these experimental data support a novel role for nuclear Hsp72 as a negative regulator of oxidative stress-induced HMGB1 cytoplasmic translocation and release.
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.