ArticleJournal of cellular and molecular medicine2014
Up-regulated HMGB1 in EAM directly led to collagen deposition by a PKCβ/Erk1/2-dependent pathway: cardiac fibroblast/myofibroblast might be another source of HMGB1.
Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Investigating the biomarkers of diabetic-cardiomyopathy with the high mobility group box-1 as a potential anti-inflammatory therapeutic target: Systematic Review and meta-analysis.Frontiers in endocrinology · 2025Pooled it
- Scoping review of preclinical and clinical studies on the role of HMGB1 in heart disease.NPJ cardiovascular health · 2026Article
- Association of Pirfenidone and its Cardioprotective effects in Pentylenetetrazole-induced kindling model of Epilepsy through the High mobility group Box-1/Toll-Like Receptor-4 pathway.Molecular biology reports · 2026Article
- The role of myocardial fibrosis in the diabetic cardiomyopathy.Diabetology & metabolic syndrome · 2025Review
- Silicate-based therapy for inflammatory dilated cardiomyopathy by inhibiting the vicious cycle of immune inflammation via FOXO signaling.Science advances · 2025Article
- HMGB1 derived from lung epithelial cells after cobalt nanoparticle exposure promotes the activation of lung fibroblasts.Nanotoxicology · 2024Article
- Cardiomyocyte Regeneration in Human Myocarditis.Biomedicines · 2024Article
- The Roles of Cardiac Fibroblasts and Endothelial Cells in Myocarditis.Frontiers in cardiovascular medicine · 2022Review
- Weighted gene co-expression network analysis identified underlying hub genes and mechanisms in the occurrence and development of viral myocarditis.Annals of translational medicine · 2020Article
- Long noncoding RNA MALAT1 sponges miR-129-5p to regulate the development of bronchopulmonary dysplasia by increasing the expression ofThe Journal of international medical research · 2020Article
- Inhibition of calpain alleviates coxsackievirus B3-induced myocarditis through suppressing the canonical NLRP3 inflammasome/caspase-1-mediated and noncanonical caspase-11-mediated pyroptosis pathways.American journal of translational research · 2020Article
- The Janus face of HMGB1 in heart disease: a necessary update.Cellular and molecular life sciences : CMLS · 2019Review
- Article
- High-Mobility Group Box 1 Mediates Fibroblast Activity via RAGE-MAPK and NF-κB Signaling in Keloid Scar Formation.International journal of molecular sciences · 2017Article
- Non-professional marathon running: RAGE axis and ST2 family changes in relation to open-window effect, inflammation and renal function.Scientific reports · 2016Article
- HMGB1 induces apoptosis and EMT in association with increased autophagy following H/R injury in cardiomyocytes.International journal of molecular medicine · 2016Article
- HMGB1 Facilitated Macrophage Reprogramming towards a Proinflammatory M1-like Phenotype in Experimental Autoimmune Myocarditis Development.Scientific reports · 2016Article
- Reduced HMGB 1-Mediated Pathway and Oxidative Stress in Resveratrol-Treated Diabetic Mice: A Possible Mechanism of Cardioprotection of Resveratrol in Diabetes Mellitus.Oxidative medicine and cellular longevity · 2016Article
- High Mobility Group Box-1: A Missing Link between Diabetes and Its Complications.Mediators of inflammation · 2016Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High mobility group box 1 (HMGB1), an important inflammatory mediator, is actively secreted by immune cells and some non-immune cells or passively released by necrotic cells. HMGB1 has been implicated in many inflammatory diseases. Our previous published data demonstrated that HMGB1 was up-regulated in heart tissue or serum in experimental autoimmune myocarditis (EAM); HMGB1 blockade could ameliorate cardiac fibrosis at the last stage of EAM. And yet, until now, no data directly showed that HMGB1 was associated with cardiac fibrosis. Therefore, the aims of the present work were to assess whether (1) up-regulated HMGB1 could directly lead to cardiac fibrosis in EAM; (2) cardiac fibroblast/myofibroblasts could secrete HMGB1 as another source of high-level HMGB1 in EAM; and (3) HMGB1 blockade could effectively prevent cardiac fibrosis at the last stage of EAM. Our results clearly demonstrated that HMGB1 could directly lead to cardiac collagen deposition, which was associated with PKCβ/Erk1/2 signalling pathway; furthermore, cardiac fibroblast/myofibroblasts could actively secrete HMGB1 under external stress; and HMGB1 secreted by cardiac fibroblasts/myofibroblasts led to cardiac fibrosis via PKCβ activation by autocrine means; HMGB1 blockade could efficiently ameliorate cardiac fibrosis in EAM mice.
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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.