ReviewAntioxidants & redox signaling2011
HMGB1 and microparticles as mediators of the immune response to cell death.
Review in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed.
- Glutamic-Alanine Rich Glycoprotein fromMarine drugs · 2024Article
- HMGB1 is a critical molecule in the pathogenesis of Gram-negative sepsis.Journal of intensive medicine · 2022Review
- Non-Coding RNA Networks as Potential Novel Biomarker and Therapeutic Target for Sepsis and Sepsis-Related Multi-Organ Failure.Diagnostics (Basel, Switzerland) · 2022Review
- Low-Grade Inflammation in the Pathogenesis of Osteoarthritis: Cellular and Molecular Mechanisms and Strategies for Future Therapeutic Intervention.Biomedicines · 2022Review
- Non-coding RNA in alcohol use disorder by affecting synaptic plasticity.Experimental brain research · 2022Review
- Fat and Protein Combat Triggers Immunological Weapons of Innate and Adaptive Immune Systems to Launch Neuroinflammation in Parkinson's Disease.International journal of molecular sciences · 2022Review
- Neuroinflammation in retinitis pigmentosa: Therapies targeting the innate immune system.Frontiers in immunology · 2022Review
- Post-Translational Modification of HMGB1 Disulfide Bonds in Stimulating and Inhibiting Inflammation.Cells · 2021Review
- Extracellular vesicle mediated feto-maternal HMGB1 signaling induces preterm birth.Lab on a chip · 2021Article
- Inflammation in osteoarthritis: is it time to dampen the alarm(in) in this debilitating disease?Clinical and experimental immunology · 2019Review
- The Destruction Of Laser-Induced Phase-Transition Nanoparticles Triggered By Low-Intensity Ultrasound: An Innovative Modality To Enhance The Immunological Treatment Of Ovarian Cancer Cells.International journal of nanomedicine · 2019Article
- Anti-tumor outcome evaluation against non-small cell lung cancer in vitro and in vivo using PolyI:C as nucleic acid therapeutic agent.American journal of translational research · 2019Article
- Promising Targets for Cancer Immunotherapy: TLRs, RLRs, and STING-Mediated Innate Immune Pathways.International journal of molecular sciences · 2017Review
- Distinct proteome pathology of circulating microparticles in systemic lupus erythematosus.Clinical proteomics · 2017Article
- The danger from within: alarmins in arthritis.Nature reviews. Rheumatology · 2016Review
- Novel concepts on pregnancy clocks and alarms: redundancy and synergy in human parturition.Human reproduction update · 2016Review
- Regulation of Posttranslational Modifications of HMGB1 During Immune Responses.Antioxidants & redox signaling · 2016Review
- Article
- Vascular Remodelling and Mesenchymal Transition in Systemic Sclerosis.Stem cells international · 2016Review
- HMGB1 in health and disease.Molecular aspects of medicine · 2014Review
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.
Funding
Abstract
In a wide variety of diseases, cell death represents both an outcome and an important step in pathogenesis. This duality occurs because cell death leads to the extracellular release of molecules and structures that can potently induce the innate immune system. These mediators include the alarmins which are endogenous cellular constituents that exit activated or dying cells to stimulate toll-like receptors (TLRs) as well as non-TLR receptors. Of alarmins, the nonhistone protein HMGB1 is the prototype. Like DNA and RNA, HMGB1 can translocate from cells as they die. The activity of HMGB1 may reflect its interaction with other molecules such as LPS, DNA, and cytokines. In addition to alarmins, dead and dying cells can release subcellular organelles called microparticles that contain cytoplasmic and nuclear constituents, including DNA and RNA. These particles can impact on many cell types to induce inflammation. The release of HMGB1 and microparticles shows important similarities, occurring with cell death as well as stimulation of certain but not all TLRs. Furthermore, nitric oxide can induce the release of both. These observations suggest that the products of dead cells can serve as important mediators to drive immune responses and promote inflammation and autoreactivity.
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.