ArticleAmerican journal of translational research2016
HMGB1 exacerbates bronchiolitis obliterans syndrome via RAGE/NF-κB/HPSE signaling to enhance latent TGF-β release from ECM.
Article in American journal of translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Time to Rethink Bronchiolitis Obliterans Syndrome Following Lung or Hematopoietic Cell Transplantation in Pediatric Patients.Cancers · 2024Review
- Discovery and development of small-molecule heparanase inhibitors.Bioorganic & medicinal chemistry · 2023Review
- Role of heparanase in ARDS through autophagy and exosome pathway (review).Frontiers in pharmacology · 2023Review
- Histone H4 induces heparan sulfate degradation by activating heparanase in chlorine gas-induced acute respiratory distress syndrome.Respiratory research · 2022Article
- Challenges in Medicinal and Aromatic Plants DNA Barcoding-Lessons from the Lamiaceae.Plants (Basel, Switzerland) · 2022Review
- MBD2 acts as a repressor to maintain the homeostasis of the Th1 program in type 1 diabetes by regulating the STAT1-IFN-γ axis.Cell death and differentiation · 2022Article
- Heparanase regulates EMT and cancer stem cell properties in prostate tumors.Frontiers in oncology · 2022Article
- Heparanase and the hallmarks of cancer.Journal of translational medicine · 2020Review
- Chronic lung allograft dysfunction post-lung transplantation: The era of bronchiolitis obliterans syndrome and restrictive allograft syndrome.World journal of transplantation · 2020Review
- Extracellular HMGB1 exacerbates autoimmune progression and recurrence of type 1 diabetes by impairing regulatory T cell stability.Diabetologia · 2020Article
- The role of innate immunity in the long-term outcome of lung transplantation.Annals of translational medicine · 2020Review
- Hydrogel-based delivery of Il-10 improves treatment of bleomycin-induced lung fibrosis in mice.Biomaterials · 2019Article
- Review
- Both conditional ablation and overexpression of E2 SUMO-conjugating enzyme (UBC9) in mouse pancreatic beta cells result in impaired beta cell function.Diabetologia · 2018Article
- Curcumin Attenuates Pulmonary Inflammation in Lipopolysaccharide Induced Acute Lung Injury in Neonatal Rat Model by Activating Peroxisome Proliferator-Activated Receptor γ (PPARγ) Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Hepatic recruitment of CD11b+Ly6C+ inflammatory monocytes promotes hepatic ischemia/reperfusion injury.International journal of molecular medicine · 2018Article
- Staphylococcus aureus Protein A induces osteoclastogenesis via the NF‑κB signaling pathway.Molecular medicine reports · 2017Article
- Gemcitabine-induced heparanase promotes aggressiveness of pancreatic cancer cells via activating EGFR signaling.Oncotarget · 2017Article
- Danger signals in regulating the immune response to solid organ transplantation.The Journal of clinical investigation · 2017Review
- Overexpression of heparanase attenuated TGF-β-stimulated signaling in tumor cells.FEBS open bio · 2017Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bronchiolitis obliterans syndrome (BOS), characterized by progressive airflow obstruction, is the main barrier to long-term graft survival after lung transplantation. Despite extensive studies, the mechanisms underlying BOS remain poorly understood, and targeted interventions have not yet been fully developed. In the present study, we employed a mouse model of tracheal transplantation and demonstrated that blockade of HMGB1 alone or combined with heparanase (HPSE) attenuates the development of BOS. It was noted that HMGB1 was first passively released from necrotic/damaged cells as a result of early unavoidable allograft injuries, leading to macrophage infiltration along with HMGB1 active secretion. Mechanistic studies revealed that extracellular HMGB1 acted through its receptor, RAGE, to activate NF-κB, which then bound to the HPSE promoter to transcribe its expression. The enhanced HPSE next released HS-bonded latent TGF-β from myofibroblast ECM by cleaving HS chains to promote the initiation and progression of BOS. Together, our data suggest that HMGB1 and HPSE could be viable targets for prevention and intervention of fibrotic diseases such BOS after lung transplantation.
Indexed as
Identifiers
27347307PMC4891412W2469354573What 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.