ArticleMolecular therapy : the journal of the American Society of Gene Therapy2013
Transcriptional profiling of HMGB1-induced myocardial repair identifies a key role for Notch signaling.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Signaling pathways regulating cardiac regeneration.Cell regeneration (London, England) · 2026Review
- Cuttlefish ink nanoparticle hydrogels ameliorate osteoarthritis via concurrent inhibition of macrophage pyroptosis and chondrocyte senescence.Journal of nanobiotechnology · 2026Article
- Scoping review of preclinical and clinical studies on the role of HMGB1 in heart disease.NPJ cardiovascular health · 2026Article
- High mobility group box 1: DAMPening the danger molecule in cardiovascular disease with exercise.Cell stress & chaperones · 2026Review
- Nicotinamide mononucleotide promotes female germline stem cell proliferation by activating the H4K16ac-Hmgb1-Fyn-PLD signaling pathway through epigenetic remodeling.Cell & bioscience · 2025Article
- Review
- The role and mechanism of HMGB1-mediated Notch1/Hes-1 pathway in anxiety and depression-like behaviors in mice with chronic rhinosinusitis.Molecular medicine (Cambridge, Mass.) · 2025Article
- Inhibition of the Notch Pathway Alleviates Nab-Paclitaxel-Induced Peripheral Neuropathic Pain in Rats by Suppressing HMGB1/Caveolin-1 Signaling in the Spinal Cord.Mediators of inflammation · 2025Article
- Signaling pathways and targeted therapy for myocardial infarction.Signal transduction and targeted therapy · 2022Review
- High Mobility Group Box 1: Biological Functions and Relevance in Oxidative Stress Related Chronic Diseases.Cells · 2022Review
- The Janus face of HMGB1 in heart disease: a necessary update.Cellular and molecular life sciences : CMLS · 2019Review
- Biomarkers identification for acute myocardial infarction detection via weighted gene co-expression network analysis.Medicine · 2017Article
- High mobility group box 1 protein attenuates myocardial ischemia reperfusion injury via inhibition of the p38 mitogen-activated protein kinase signaling pathway.Experimental and therapeutic medicine · 2017Article
- Notch Signaling in Ischemic Damage and Fibrosis: Evidence and Clues from the Heart.Frontiers in pharmacology · 2017Review
- rhHMGB1 drives osteoblast migration in a TLR2/TLR4- and NF-κB-dependent manner.Bioscience reports · 2016Article
- c-kit(+) cells: the tell-tale heart of cardiac regeneration?Cellular and molecular life sciences : CMLS · 2015Review
- High-mobility group box 1: a novel target for treatment of Pseudomonas aeruginosa keratitis.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- DAMPs from Cell Death to New Life.Frontiers in immunology · 2015Review
- HMGB1 in health and disease.Molecular aspects of medicine · 2014Review
- The role of notch in the cardiovascular system: potential adverse effects of investigational notch inhibitors.Frontiers in oncology · 2014Review
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exogenous high-mobility group box 1 protein (HMGB1) administration to the mouse heart, during acute myocardial infarction (MI), results in cardiac regeneration via resident c-kit(+) cell (CPC) activation. Aim of the present study was to identify the molecular pathways involved in HMGB1-induced heart repair. Gene expression profiling was performed to identify differentially expressed genes in the infarcted and bordering regions of untreated and HMGB1-treated mouse hearts, 3 days after MI. Functional categorization of the transcripts, accomplished using Ingenuity Pathway Analysis software (IPA), revealed that genes involved in tissue regeneration, that is, cardiogenesis, vasculogenesis and angiogenesis, were present both in the infarcted area and in the peri-infarct zone; HMGB1 treatment further increased the expression of these genes. IPA revealed the involvement of Notch signaling pathways in HMGB1-treated hearts. Importantly, HMGB1 determined a 35 and 58% increase in cardiomyocytes and CPCs expressing Notch intracellular cytoplasmic domain, respectively. Further, Notch inhibition by systemic treatment with the γ-secretase inhibitor DAPT, which blocked the proteolytic activation of Notch receptors, reduced the number of CPCs, their proliferative fraction, and cardiomyogenic differentiation in HMGB1-treated infarcted hearts. The present study gives insight into the molecular processes involved in HMGB1-mediated cardiac regeneration and indicates Notch signaling as a key player.
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