ArticleArteriosclerosis, thrombosis, and vascular biology2015
HMGB1-Driven Inflammation and Intimal Hyperplasia After Arterial Injury Involves Cell-Specific Actions Mediated by TLR4.
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Article in Arteriosclerosis, thrombosis, and vascular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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41citing papers in PubMed
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41 citing papers in PubMed, 70 citations in OpenAlex.
- The Nitinol Stented Vessels: Integrating Pathological Triad of Inflammation, Hypoxia and Mechanical Stress to Rethink Endothelial Protection.Stem cell reviews and reports · 2026Article
- HMGB1 as a danger signal in vascular remodeling.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Review
- TRIM24 Impediment suppresses VSMC modulation and attenuates neointimal hyperplasia via redox and autophagy pathways.Molecular biology reports · 2026Article
- Deciphering and Targeting the Schwannoma-Neuron-Macrophage Crosstalk for the Treatment of Schwannomatosis and Associated Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The redox-sensitive protein HMGB1: intracellular and extracellular roles.Experimental & molecular medicine · 2026Review
- HMGB1: key mediator in digestive system diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Intravascular delivery of an MK2 inhibitory peptide to prevent restenosis after angioplasty.Biomaterials · 2025Article
- Ganglioside GA2-mediated caspase-11 activation drives macrophage pyroptosis aggravating intimal hyperplasia after arterial injury.International journal of biological sciences · 2025Article
- High Mobility Group Box 1 (HMGB1): Molecular Signaling and Potential Therapeutic Strategies.Cells · 2024Review
- Target Gene-Based Association Study of High Mobility Group Box Protein 1 in Intracranial Aneurysms in Koreans.Brain sciences · 2024Article
- Biophysically stressed vascular smooth muscle cells express MCP-1The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024Article
- Thiocarbazate building blocks enable the construction of azapeptides for rapid development of therapeutic candidates.Nature communications · 2022Article
- Extracellular HMGB1 as Inflammatory Mediator in the Progression of Mycoplasma Gallisepticum Infection.Cells · 2022Article
- Doxorubicin induced immune abnormalities and inflammatory responses via HMGB1, HIF1-α and VEGF pathway in progressive of cardiovascular damage.Annals of medicine and surgery (2012) · 2022Review
- Recent advances in Extracellular Vesicles and their involvements in vasculitis.Free radical biology & medicine · 2021Review
- GSDME-mediated pyroptosis promotes inflammation and fibrosis in obstructive nephropathy.Cell death and differentiation · 2021Article
- Sterile inflammation in the pathogenesis of maturation failure of arteriovenous fistula.Journal of molecular medicine (Berlin, Germany) · 2021Review
- 5-LO-derived LTB4 plays a key role in MCP-1 expression in HMGB1-exposed VSMCs via a BLTR1 signaling axis.Scientific reports · 2021Article
- Integrin α9 regulates smooth muscle cell phenotype switching and vascular remodeling.JCI insight · 2021Article
- The HIV protease inhibitor Saquinavir attenuates sepsis-induced acute lung injury and promotes M2 macrophage polarization via targeting matrix metalloproteinase-9.Cell death & disease · 2021Article
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Authors and funding
17 authors at 1 institution in 1 country.
Jingjing CaiFrom the Center of Clinical Pharmacology of the Third Xiangya Hospital (J.C., H.Y., Q.W., Z.H., J. Wu), the Center of Vascular Disease and Translational Medicine (A.F.C.), Department of Cardiology of the Third Xiangya Hospital (J.C., H.Y., W.J., K.Y.), and Department of Hematology of the Third Xiangya Hospital (B.L.), Central South University, Changsha, China; Department of Surgery, University of Pittsburgh School of Medicine, PA (J.C., Q.W., Z.H., J. Wang, D.C., J. Wu, J.P.P., D.J.H., T.R.B., A.F.C.); and Laboratory of Biomedical Science, the Feinstein Institute for Medical Research, Manhasset, New York (H.Y., Y.A.-A., K.J.T.).
Hong YuanFrom the Center of Clinical Pharmacology of the Third Xiangya Hospital (J.C., H.Y., Q.W., Z.H., J. Wu), the Center of Vascular Disease and Translational Medicine (A.F.C.), Department of Cardiology of the Third Xiangya Hospital (J.C., H.Y., W.J., K.Y.), and Department of Hematology of the Third Xiangya Hospital (B.L.), Central South University, Changsha, China; Department of Surgery, University of Pittsburgh School of Medicine, PA (J.C., Q.W., Z.H., J. Wang, D.C., J. Wu, J.P.P., D.J.H., T.R.B., A.F.C.); and Laboratory of Biomedical Science, the Feinstein Institute for Medical Research, Manhasset, New York (H.Y., Y.A.-A., K.J.T.).
Qingde WangFrom the Center of Clinical Pharmacology of the Third Xiangya Hospital (J.C., H.Y., Q.W., Z.H., J. Wu), the Center of Vascular Disease and Translational Medicine (A.F.C.), Department of Cardiology of the Third Xiangya Hospital (J.C., H.Y., W.J., K.Y.), and Department of Hematology of the Third Xiangya Hospital (B.L.), Central South University, Changsha, China; Department of Surgery, University of Pittsburgh School of Medicine, PA (J.C., Q.W., Z.H., J. Wang, D.C., J. Wu, J.P.P., D.J.H., T.R.B., A.F.C.); and Laboratory of Biomedical Science, the Feinstein Institute for Medical Research, Manhasset, New York (H.Y., Y.A.-A., K.J.T.).
Huan YangFrom the Center of Clinical Pharmacology of the Third Xiangya Hospital (J.C., H.Y., Q.W., Z.H., J. Wu), the Center of Vascular Disease and Translational Medicine (A.F.C.), Department of Cardiology of the Third Xiangya Hospital (J.C., H.Y., W.J., K.Y.), and Department of Hematology of the Third Xiangya Hospital (B.L.), Central South University, Changsha, China; Department of Surgery, University of Pittsburgh School of Medicine, PA (J.C., Q.W., Z.H., J. Wang, D.C., J. Wu, J.P.P., D.J.H., T.R.B., A.F.C.); and Laboratory of Biomedical Science, the Feinstein Institute for Medical Research, Manhasset, New York (H.Y., Y.A.-A., K.J.T.).
Yousef Al-AbedFrom the Center of Clinical Pharmacology of the Third Xiangya Hospital (J.C., H.Y., Q.W., Z.H., J. Wu), the Center of Vascular Disease and Translational Medicine (A.F.C.), Department of Cardiology of the Third Xiangya Hospital (J.C., H.Y., W.J., K.Y.), and Department of Hematology of the Third Xiangya Hospital (B.L.), Central South University, Changsha, China; Department of Surgery, University of Pittsburgh School of Medicine, PA (J.C., Q.W., Z.H., J. Wang, D.C., J. Wu, J.P.P., D.J.H., T.R.B., A.F.C.); and Laboratory of Biomedical Science, the Feinstein Institute for Medical Research, Manhasset, New York (H.Y., Y.A.-A., K.J.T.).
Zhong HuaFrom the Center of Clinical Pharmacology of the Third Xiangya Hospital (J.C., H.Y., Q.W., Z.H., J. Wu), the Center of Vascular Disease and Translational Medicine (A.F.C.), Department of Cardiology of the Third Xiangya Hospital (J.C., H.Y., W.J., K.Y.), and Department of Hematology of the Third Xiangya Hospital (B.L.), Central South University, Changsha, China; Department of Surgery, University of Pittsburgh School of Medicine, PA (J.C., Q.W., Z.H., J. Wang, D.C., J. Wu, J.P.P., D.J.H., T.R.B., A.F.C.); and Laboratory of Biomedical Science, the Feinstein Institute for Medical Research, Manhasset, New York (H.Y., Y.A.-A., K.J.T.).
Jiemei WangFrom the Center of Clinical Pharmacology of the Third Xiangya Hospital (J.C., H.Y., Q.W., Z.H., J. Wu), the Center of Vascular Disease and Translational Medicine (A.F.C.), Department of Cardiology of the Third Xiangya Hospital (J.C., H.Y., W.J., K.Y.), and Department of Hematology of the Third Xiangya Hospital (B.L.), Central South University, Changsha, China; Department of Surgery, University of Pittsburgh School of Medicine, PA (J.C., Q.W., Z.H., J. Wang, D.C., J. Wu, J.P.P., D.J.H., T.R.B., A.F.C.); and Laboratory of Biomedical Science, the Feinstein Institute for Medical Research, Manhasset, New York (H.Y., Y.A.-A., K.J.T.).
Dandan ChenFrom the Center of Clinical Pharmacology of the Third Xiangya Hospital (J.C., H.Y., Q.W., Z.H., J. Wu), the Center of Vascular Disease and Translational Medicine (A.F.C.), Department of Cardiology of the Third Xiangya Hospital (J.C., H.Y., W.J., K.Y.), and Department of Hematology of the Third Xiangya Hospital (B.L.), Central South University, Changsha, China; Department of Surgery, University of Pittsburgh School of Medicine, PA (J.C., Q.W., Z.H., J. Wang, D.C., J. Wu, J.P.P., D.J.H., T.R.B., A.F.C.); and Laboratory of Biomedical Science, the Feinstein Institute for Medical Research, Manhasset, New York (H.Y., Y.A.-A., K.J.T.).
Jinze WuFrom the Center of Clinical Pharmacology of the Third Xiangya Hospital (J.C., H.Y., Q.W., Z.H., J. Wu), the Center of Vascular Disease and Translational Medicine (A.F.C.), Department of Cardiology of the Third Xiangya Hospital (J.C., H.Y., W.J., K.Y.), and Department of Hematology of the Third Xiangya Hospital (B.L.), Central South University, Changsha, China; Department of Surgery, University of Pittsburgh School of Medicine, PA (J.C., Q.W., Z.H., J. Wang, D.C., J. Wu, J.P.P., D.J.H., T.R.B., A.F.C.); and Laboratory of Biomedical Science, the Feinstein Institute for Medical Research, Manhasset, New York (H.Y., Y.A.-A., K.J.T.).
Ben LuFrom the Center of Clinical Pharmacology of the Third Xiangya Hospital (J.C., H.Y., Q.W., Z.H., J. Wu), the Center of Vascular Disease and Translational Medicine (A.F.C.), Department of Cardiology of the Third Xiangya Hospital (J.C., H.Y., W.J., K.Y.), and Department of Hematology of the Third Xiangya Hospital (B.L.), Central South University, Changsha, China; Department of Surgery, University of Pittsburgh School of Medicine, PA (J.C., Q.W., Z.H., J. Wang, D.C., J. Wu, J.P.P., D.J.H., T.R.B., A.F.C.); and Laboratory of Biomedical Science, the Feinstein Institute for Medical Research, Manhasset, New York (H.Y., Y.A.-A., K.J.T.).
John P PribisFrom the Center of Clinical Pharmacology of the Third Xiangya Hospital (J.C., H.Y., Q.W., Z.H., J. Wu), the Center of Vascular Disease and Translational Medicine (A.F.C.), Department of Cardiology of the Third Xiangya Hospital (J.C., H.Y., W.J., K.Y.), and Department of Hematology of the Third Xiangya Hospital (B.L.), Central South University, Changsha, China; Department of Surgery, University of Pittsburgh School of Medicine, PA (J.C., Q.W., Z.H., J. Wang, D.C., J. Wu, J.P.P., D.J.H., T.R.B., A.F.C.); and Laboratory of Biomedical Science, the Feinstein Institute for Medical Research, Manhasset, New York (H.Y., Y.A.-A., K.J.T.).
Weihong JiangFrom the Center of Clinical Pharmacology of the Third Xiangya Hospital (J.C., H.Y., Q.W., Z.H., J. Wu), the Center of Vascular Disease and Translational Medicine (A.F.C.), Department of Cardiology of the Third Xiangya Hospital (J.C., H.Y., W.J., K.Y.), and Department of Hematology of the Third Xiangya Hospital (B.L.), Central South University, Changsha, China; Department of Surgery, University of Pittsburgh School of Medicine, PA (J.C., Q.W., Z.H., J. Wang, D.C., J. Wu, J.P.P., D.J.H., T.R.B., A.F.C.); and Laboratory of Biomedical Science, the Feinstein Institute for Medical Research, Manhasset, New York (H.Y., Y.A.-A., K.J.T.).
Kan YangFrom the Center of Clinical Pharmacology of the Third Xiangya Hospital (J.C., H.Y., Q.W., Z.H., J. Wu), the Center of Vascular Disease and Translational Medicine (A.F.C.), Department of Cardiology of the Third Xiangya Hospital (J.C., H.Y., W.J., K.Y.), and Department of Hematology of the Third Xiangya Hospital (B.L.), Central South University, Changsha, China; Department of Surgery, University of Pittsburgh School of Medicine, PA (J.C., Q.W., Z.H., J. Wang, D.C., J. Wu, J.P.P., D.J.H., T.R.B., A.F.C.); and Laboratory of Biomedical Science, the Feinstein Institute for Medical Research, Manhasset, New York (H.Y., Y.A.-A., K.J.T.).
David J HackamFrom the Center of Clinical Pharmacology of the Third Xiangya Hospital (J.C., H.Y., Q.W., Z.H., J. Wu), the Center of Vascular Disease and Translational Medicine (A.F.C.), Department of Cardiology of the Third Xiangya Hospital (J.C., H.Y., W.J., K.Y.), and Department of Hematology of the Third Xiangya Hospital (B.L.), Central South University, Changsha, China; Department of Surgery, University of Pittsburgh School of Medicine, PA (J.C., Q.W., Z.H., J. Wang, D.C., J. Wu, J.P.P., D.J.H., T.R.B., A.F.C.); and Laboratory of Biomedical Science, the Feinstein Institute for Medical Research, Manhasset, New York (H.Y., Y.A.-A., K.J.T.).
Kevin J TraceyFrom the Center of Clinical Pharmacology of the Third Xiangya Hospital (J.C., H.Y., Q.W., Z.H., J. Wu), the Center of Vascular Disease and Translational Medicine (A.F.C.), Department of Cardiology of the Third Xiangya Hospital (J.C., H.Y., W.J., K.Y.), and Department of Hematology of the Third Xiangya Hospital (B.L.), Central South University, Changsha, China; Department of Surgery, University of Pittsburgh School of Medicine, PA (J.C., Q.W., Z.H., J. Wang, D.C., J. Wu, J.P.P., D.J.H., T.R.B., A.F.C.); and Laboratory of Biomedical Science, the Feinstein Institute for Medical Research, Manhasset, New York (H.Y., Y.A.-A., K.J.T.).
Timothy R BilliarFrom the Center of Clinical Pharmacology of the Third Xiangya Hospital (J.C., H.Y., Q.W., Z.H., J. Wu), the Center of Vascular Disease and Translational Medicine (A.F.C.), Department of Cardiology of the Third Xiangya Hospital (J.C., H.Y., W.J., K.Y.), and Department of Hematology of the Third Xiangya Hospital (B.L.), Central South University, Changsha, China; Department of Surgery, University of Pittsburgh School of Medicine, PA (J.C., Q.W., Z.H., J. Wang, D.C., J. Wu, J.P.P., D.J.H., T.R.B., A.F.C.); and Laboratory of Biomedical Science, the Feinstein Institute for Medical Research, Manhasset, New York (H.Y., Y.A.-A., K.J.T.).
Alex F ChenFrom the Center of Clinical Pharmacology of the Third Xiangya Hospital (J.C., H.Y., Q.W., Z.H., J. Wu), the Center of Vascular Disease and Translational Medicine (A.F.C.), Department of Cardiology of the Third Xiangya Hospital (J.C., H.Y., W.J., K.Y.), and Department of Hematology of the Third Xiangya Hospital (B.L.), Central South University, Changsha, China; Department of Surgery, University of Pittsburgh School of Medicine, PA (J.C., Q.W., Z.H., J. Wang, D.C., J. Wu, J.P.P., D.J.H., T.R.B., A.F.C.); and Laboratory of Biomedical Science, the Feinstein Institute for Medical Research, Manhasset, New York (H.Y., Y.A.-A., K.J.T.). afychen@yahoo.com billiartr@upmc.edu.
University of Pittsburgh · US
Funding
University of Pittsburgh Clinical and Translational Science InstituteUL1TR000005 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REIS, STEVEN E · 2012 to 2015
$50.8MRegulation and Function of Endotoxin Signaling in Surgical SepsisR01GM050441 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BILLIAR, TIMOTHY R · 1994 to 2018
$4.6MTLR4 Signaling in the Pathogenesis of Surgical Necrotizing EnterocolitisR01GM078238 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HACKAM, DAVID J · 2006 to 2019
$3.9MModulation of TLR4 and TLR9 Signaling in NECR01DK083752 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HACKAM, DAVID J · 2008 to 2016
$3.4MNCATS NIH HHS UL1 TR000005NIDDK NIH HHS R01 DK083752NIGMS NIH HHS R01 GM050441NIGMS NIH HHS R01 GM078238NIGMS NIH HHS R01 GM50441
Abstract
objectiveEndoluminal vascular interventions such as angioplasty initiate a sterile inflammatory response resulting from local tissue damage. This response drives the development of intimal hyperplasia (IH) that, in turn, can lead to arterial occlusion. We hypothesized that the ubiquitous nuclear protein and damage-associated molecular pattern molecule, high-mobility group box 1 (HMGB1), is one of the endogenous mediators that activates processes leading to IH after endoluminal injury to the arterial wall. The aim of this study is to investigate whether approaches that reduce the levels of HMGB1 or inhibit its activity suppresses IH after arterial injury. APPROACH AND
resultsHere, we show that HMGB1 regulates IH in a mouse carotid wire injury model. Induced genetic deletion or neutralization of HMGB1 prevents IH, monocyte recruitment, and smooth muscle cell growth factor production after endoluminal carotid artery injury. A specific inhibitor of HMGB1 myeloid differentiation factor 2-toll-like receptor 4 (TLR4) interaction, P5779, also significantly inhibits IH. HMGB1 deletion is mimicked in this model by global deletion of TLR4 and partially replicated by myeloid-specific deletion of TLR4 but not TLR2 or receptor for advanced glycation endproducts deletion. The specific HMGB1 isoform known to activate TLR4 signaling (disulfide HMGB1) stimulates smooth muscle cell to migrate and produce monocyte chemotactic protein 1/CCL2) via TLR4. Macrophages produce smooth muscle cell mitogens in response to disulfide HMGB1 also in a TLR4/myeloid differentiation primary response gene (88)/Trif-dependent manner.
conclusionsThese findings place HMGB1 and its receptor, TLR4 as critical regulators of the events that drive the inflammation leading to IH after endoluminal arterial injury and identify this pathway as a possible therapeutic target to limit IH to attenuate damage-associated molecular pattern molecule-mediated vascular inflammatory responses.
Indexed as
NeointimaAdaptor Proteins, Vesicular TransportAnimalsCarotid ArteriesCarotid Artery InjuriesCell MovementCell ProliferationCells, CulturedChemotaxis, LeukocyteCytokinesDisease Models, AnimalHMGB1 ProteinHumansHyperplasiaInflammation MediatorsMacrophages, PeritonealAdaptor Proteins, Vesicular TransportCytokinesHMGB1 ProteinHMGB1 protein, humanHMGB1 protein, mouseInflammation MediatorsMyd88 protein, mouseMyeloid Differentiation Factor 88Ticam1 protein, mouseTLR4 protein, humanTlr4 protein, mouseToll-Like Receptor 4angioplastycarotid artery injuriesHMGBI proteinhyperplasiamacrophages
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