ArticleFASEB bioAdvances2022
The roles of HMGB1-produced DNA gaps in DNA protection and aging biomarker reversal.
Article in FASEB bioAdvances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 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
19 citing papers in PubMed, 28 citations in OpenAlex.
- Box A of HMGB1 plasmid reverses the age-related changes in the plasma proteomic profile of perimenopausal monkeys.Scientific reports · 2026Article
- Characterization and stability of plasmid DNA calcium nanoparticles using a simple formulation for gene therapy.Scientific reports · 2025Article
- A conceptual model of oxygen-ozone therapy as a modulator of aging via the HMGB1 pathway.Biogerontology · 2025Review
- HMGB1 Box A gene therapy to alleviate bleomycin-induced pulmonary fibrosis in rats.BMC pulmonary medicine · 2025Article
- The role of Box A of HMGB1 in producing γH2AX associated DNA breaks in lung cancer.Scientific reports · 2025Article
- HMGB1-BoxA gene therapy in reversing cisplatin resistance in non-small cell lung cancer.PloS one · 2025Article
- Unveiling senescence-associated ocular pathogenesis via lacrimal gland organoid magnetic bioassembly platform and HMGB1-Box A gene therapy.Scientific reports · 2024Article
- The role of high mobility group proteins in cellular senescence mechanisms.Frontiers in aging · 2024Review
- Targeting Neutrophil Extracellular Traps in Gouty Arthritis: Insights into Pathogenesis and Therapeutic Potential.Journal of inflammation research · 2024Review
- The inverse association between DNA gaps and HbA1c levels in type 2 diabetes mellitus.Scientific reports · 2023Article
- Decreased Alu methylation in type 2 diabetes mellitus patients increases HbA1c levels.Journal of clinical laboratory analysis · 2023Article
- Targeting HMGB1: A Potential Therapeutic Strategy for Chronic Kidney Disease.International journal of biological sciences · 2023Review
- The roles of HMGB1-produced DNA gaps in DNA protection and aging biomarker reversal.FASEB bioAdvances · 2022Article
- Article
- Magnetic bioassembly platforms for establishing craniofacial exocrine gland organoids as aging in vitro models.PloS one · 2022Article
- Secretome from HMGB1 Box A-over-expressing Adipose-derived Stem Cells Shows Potential for Skin Rejuvenation by Senescence Reversal in PM2.5-induced Senescence CellsIn vivo (Athens, Greece)Article
- Box A of HMGB1 Maintains the DNA Gap and Prevents DDR-induced Kidney Injury in D-galactose Induction Rats.In vivo (Athens, Greece)Article
- Long-term Safety Pharmacology and Musculoskeletal Changes of HMGB1 Box A Gene Therapy in Middle-aged Monkeys.In vivo (Athens, Greece)Article
- The Role of Box A ofIn vivo (Athens, Greece)Article
Corrections and comments
- Erratum issued
Authors and funding
23 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The endogenous DNA damage triggering an aging progression in the elderly is prevented in the youth, probably by naturally occurring DNA gaps. Decreased DNA gaps are found during chronological aging in yeast. So we named the gaps "Youth-DNA-GAPs." The gaps are hidden by histone deacetylation to prevent DNA break response and were also reduced in cells lacking either the high-mobility group box (HMGB) or the NAD-dependent histone deacetylase, SIR2. A reduction in DNA gaps results in shearing DNA strands and decreasing cell viability. Here, we show the roles of DNA gaps in genomic stability and aging prevention in mammals. The number of Youth-DNA-GAPs were low in senescent cells, two aging rat models, and the elderly. Box A domain of HMGB1 acts as molecular scissors in producing DNA gaps. Increased gaps consolidated DNA durability, leading to DNA protection and improved aging features in senescent cells and two aging rat models similar to those of young organisms. Like the naturally occurring Youth-DNA-GAPs, Box A-produced DNA gaps avoided DNA double-strand break response by histone deacetylation and SIRT1, a Sir2 homolog. In conclusion, Youth-DNA-GAPs are a biomarker determining the DNA aging stage (young/old). Box A-produced DNA gaps ultimately reverse aging features. Therefore, DNA gap formation is a potential strategy to monitor and treat aging-associated diseases.
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.