ArticleHypertension (Dallas, Tex. : 1979)2020
Necrosis-Released HMGB1 (High Mobility Group Box 1) in the Progressive Pulmonary Arterial Hypertension Associated With Male Sex.
Article in Hypertension (Dallas, Tex. : 1979), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- Antiviral and immunomodulatory effect of zapnometinib in animal models and hospitalized COVID-19 patients.Frontiers in immunology · 2025Trial
- Beyond the Heart-Lung Axis: A Review of the Crosstalk Between the Hemodynamic, Neurohormonal, and Immune Systems in Pulmonary Hypertension.Comprehensive physiology · 2026Review
- Exposure Pattern Determines Methamphetamine-Induced Right Ventricular Dysfunction and Vascular Remodeling.Comprehensive Physiology · 2026Article
- Context-dependent release of HMGB1: cell death mode, cell type and LPS stress drive monomer and heterocomplex formation.Molecular medicine (Cambridge, Mass.) · 2026Article
- Neonatal pulmonary vascular remodeling induced by increased blood flow is associated with an antiviral-like immune signature.Frontiers in immunology · 2026Article
- The Critical Role of HMGB1Cys106 in Regulating Sex-Specific p53 Signaling in Pulmonary Arterial Hypertension.American journal of respiratory cell and molecular biology · 2025Article
- Engineering HMGB1-derived Peptides to Unravel Sex-Specific Mechanisms in Pulmonary Arterial Hypertension.American journal of respiratory cell and molecular biology · 2025Article
- New insights into pulmonary arterial hypertension: interaction between PANoptosis and perivascular inflammatory responses.Apoptosis : an international journal on programmed cell death · 2025Review
- HMGB1 drives T-cell activation in hypertensive males and females.American journal of physiology. Renal physiology · 2025Article
- Exploring the diagnostic and immune infiltration roles of disulfidptosis related genes in pulmonary hypertension.Respiratory research · 2024Article
- Circulating free heme induces cytokine storm and pulmonary hypertension through the MKK3/p38 axis.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Targeting necroptosis: a promising avenue for respiratory disease treatment.Cell communication and signaling : CCS · 2024Review
- Molecular regulation and therapeutic implications of cell death in pulmonary hypertension.Cell death discovery · 2023Review
- HMGB1-induced activation of ER stress contributes to pulmonary artery hypertension in vitro and in vivo.Respiratory research · 2023Article
- Association of HMGB1 levels in synovial fluid with the severity of temporomandibular joint osteoarthritis.BMC musculoskeletal disorders · 2023Article
- The mechanism of programmed death and endoplasmic reticulum stress in pulmonary hypertension.Cell death discovery · 2023Review
- Interleukin-6 and pulmonary hypertension: from physiopathology to therapy.Frontiers in immunology · 2023Review
- Cytokine profiling in pulmonary arterial hypertension: the role of redox homeostasis and sex.Translational research : the journal of laboratory and clinical medicine · 2022Article
- Analysis of necroptosis and its association with pyroptosis in organ damage in experimental pulmonary arterial hypertension.Journal of cellular and molecular medicine · 2022Article
- The role of necroptosis in common respiratory diseases in children.Frontiers in pediatrics · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Damage-associated molecular patterns, such as HMGB1 (high mobility group box 1), play a well-recognized role in the development of pulmonary arterial hypertension (PAH), a progressive fatal disease of the pulmonary vasculature. However, the contribution of the particular type of vascular cells, type of cell death, or the form of released HMGB1 in PAH remains unclear. Moreover, although male patients with PAH show a higher level of circulating HMGB1, its involvement in the severe PAH phenotype reported in males is unknown. In this study, we aimed to investigate the sources and active forms of HMGB1 released from damaged vascular cells and their contribution to the progressive type of PAH in males. Our results showed that HMGB1 is released by either pulmonary artery human endothelial cells or human pulmonary artery smooth muscle cells that underwent necrotic cell death, although only human pulmonary artery smooth muscle cells produce HMGB1 during apoptosis. Moreover, only human pulmonary artery smooth muscle cell death induced a release of dimeric HMGB1, found to be mitochondrial reactive oxygen species dependent, and TLR4 (toll-like receptor 4) activation. The modified Sugen/Hypoxia rat model replicates the human sexual dimorphism in PAH severity (right ventricle systolic pressure in males versus females 54.7±2.3 versus 44.6±2 mm Hg). By using this model, we confirmed that necroptosis and necrosis are the primary sources of circulating HMGB1 in the male rats, although only necrosis increased circulation of HMGB1 dimers. Attenuation of necrosis but not apoptosis or necroptosis prevented TLR4 activation in males and blunted the sex differences in PAH severity. We conclude that necrosis, through the release of HMGB1 dimers, predisposes males to a progressive form of PAH.
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