ArticleJournal of cellular and molecular medicine2018
HMGB1 deficiency reduces H
Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
What it found
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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
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Superoxide Dismutase Administration: A Review of Proposed Human Uses.Molecules (Basel, Switzerland) · 2021Pooled it
- Pharmacological Mechanisms of Active Constituents from Traditional Chinese Medicine for Vitiligo Treatment.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Sappanone A exerted promising therapeutic effects in vitiligo through Wnt5a-mediated noncanonical Wnt signaling.Journal of natural medicines · 2026Article
- Vitiligo as a Failure of Immune Resolution and Tissue Regeneration: From Stress Signals to Targeted Immune Modulation.Clinical reviews in allergy & immunology · 2026Review
- Curcumin Inhibits Lipopolysaccharide-Induced Inflammation Through the HMGB1/NF-κB Signaling Pathway to Promote the Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells.Molecular biotechnology · 2026Article
- Independent and interactive roles of hirudin and HMGB1 interference in protecting renal function by regulating autophagy, apoptosis, and kidney injury in chronic kidney disease.European journal of histochemistry : EJH · 2025Article
- Rosuvastatin ameliorates chemically induced acute lung injury in rats by targeting ferroptosis, heat shock protein B1, and inflammation.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Updates on the Role of Innate Immunity's Pattern Recognition Receptors in Vitiligo Pathogenesis and Therapeutic Potential.Clinical, cosmetic and investigational dermatology · 2025Review
- Alterations inContemporary oncology (Poznan, Poland) · 2025Article
- Co-regulatory mechanisms and potential markers of oxidative stress-related genes in vitiligo and alopecia areata.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024Article
- Identification and validation of RNA-binding protein SLC3A2 regulates melanocyte ferroptosis in vitiligo by integrated analysis of single-cell and bulk RNA-sequencing.BMC genomics · 2024Article
- Oxidative Stress and Potential Antioxidant Therapies in Vitiligo: A Narrative Review.Molecular diagnosis & therapy · 2023Review
- NRF2 in the Epidermal Pigmentary System.Biomolecules · 2022Review
- Current Understanding of the Role of Senescent Melanocytes in Skin Ageing.Biomedicines · 2022Review
- Damage-associated molecular patterns in vitiligo: igniter fuse from oxidative stress to melanocyte loss.Redox report : communications in free radical research · 2022Review
- Current Concepts of Vitiligo Immunopathogenesis.Biomedicines · 2022Review
- Cell type-specific response of colon cancer tumor cell lines to oncolytic HSV-1 virotherapy in hypoxia.Cancer cell international · 2022Article
- Oxeiptosis: a novel pathway of melanocytes death in response to oxidative stress in vitiligo.Cell death discovery · 2022Article
- The Role of Oxidative Stress in the Pathogenesis of Vitiligo: A Culprit for Melanocyte Death.Oxidative medicine and cellular longevity · 2022Review
- Research Progress on Targeted Antioxidant Therapy and Vitiligo.Oxidative medicine and cellular longevity · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress leads to melanocyte death and has been implicated in the pathogenesis of vitiligo. The nuclear factor, E2-related factor 2 (Nrf2), is a critical transcription factor in protecting cells from oxidative damage. High-mobility group box 1 (HMGB1) is a chromatin-associated nuclear protein and an extracellular damage-associated molecular pattern molecule. Extracellular HMGB1 released from activated immune cells, necrotic or injured cells, becomes a proinflammatory mediator through binding to cell-surface receptors of responding cells. In this study, we investigated the role of HMGB1 from melanocytes in the response to oxidative stress and the mechanism involved. We showed that HMGB1 is expressed by primary normal human epidermal melanocytes (NHEMs). H
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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.