Haihong Zhang
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Also affiliated: Agency for Science, Technology and Research (2023); Qinghai University (2024); Fujian Medical University (2024–2026); Arkansas Children's Hospital (2016–2020); China National Offshore Oil Corporation (China) (2025); Chinese Academy of Medical Sciences & Peking Union Medical College (2022); Peking University (2009–2024); Sichuan University (2023); Fudan University (2019); Chinese PLA General Hospital (2015); Institute for Infocomm Research (2023); Qinghai University Affiliated Hospital (2024); West China Hospital of Sichuan University (2023); Shanghai Children's Medical Center (2024–2026); Lanzhou University Second Hospital (2024–2026); Tang Du Hospital (2019); Chinese People's Liberation Army (2015); Aviation General Hospital (2024); Fu Wai Hospital (2022); Institute of Basic Medical Sciences of the Chinese Academy of Medical Sciences (2022); State Key Laboratory of Cardiovascular Disease (2022); State Key Laboratory of Medical Molecular Biology (2022); State Key Laboratory of Genetic Engineering (2019); Arkansas Children's Research Institute (2021–2026); Lanzhou University (2024–2026); Air Force Medical University (2019)
Research Areas
Biomedical Subjects
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Biography and Research Information
OverviewAI-generated summary
Haihong Zhang's research focuses on understanding the molecular mechanisms underlying various diseases, particularly those involving cell proliferation and vascular malformations. Recent publications explore the role of matrix metalloproteinases in the progression of arteriovenous malformations and the expression of beta-adrenergic receptor subtypes in infantile hemangiomas, including their response to propranolol. Zhang also investigates the interaction between gastric carcinoma cells and neural cells, identifying pathways that promote perineural invasion. Further research examines the involvement of the NOTCH pathway in infantile hemangiomas and the role of PKM2 in macrophage phagocytosis and atherosclerosis. Collaborating with researchers at the University of Arkansas for Medical Sciences, including Gresham T. Richter and Graham M. Strub, Zhang has contributed to 50 publications with an h-index of 12 and over 450 citations.
Metrics
- h-index: 12
- Publications: 49
- Citations: 454
Selected Publications
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M2 Macrophage Polarization Characterizes an Immunosuppressive Microenvironment in Extracranial Arteriovenous Malformations (2026)
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Rescue of Angiopoietin‐2 Inhibits Proliferation of Lymphatic Malformation Endothelial Cells (2025)
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Mural Cells Initiate Endothelial-to-Mesenchymal Transition in Adjacent Endothelial Cells in Extracranial AVMs (2024)
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Quantitative plasma proteomic analysis in children after superior cavopulmonary anastomosis with pulmonary arteriovenous malformations (2024)
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Upregulated MicroRNA-21 Drives the Proliferation of Lymphatic Malformation Endothelial Cells by Inhibiting PDCD4 (2023)
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Extracranial arteriovenous malformations demonstrate dysregulated TGF-β/BMP signaling and increased circulating TGF-β1 (2022)
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Extracranial arteriovenous malformations demonstrate dysregulated TGF-β/BMP signaling and increased circulating TGF-β1 (2022)
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Presence of estrogen and progesterone receptors in proliferating and involuting infantile hemangiomas (2021)
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NOTCH pathway activation in infantile hemangiomas (2020)
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Abnormal elastin and collagen deposition is present in extracranial arteriovenous malformations: A comparison to intracranial disease. (2019)
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The expression of renin–angiotensin–aldosterone axis components in infantile hemangioma tissue and the impact of propranolol treatment (2017)
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Expression of β-Adrenergic Receptor Subtypes in Proliferative, Involuted, and Propranolol-Responsive Infantile Hemangiomas (2016)
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Elevated Expression of Matrix Metalloproteinase-9 not Matrix Metalloproteinase-2 Contributes to Progression of Extracranial Arteriovenous Malformation (2016)
Collaboration Network
Top Collaborators
- Elevated Expression of Matrix Metalloproteinase-9 not Matrix Metalloproteinase-2 Contributes to Progression of Extracranial Arteriovenous Malformation
- Expression of β-Adrenergic Receptor Subtypes in Proliferative, Involuted, and Propranolol-Responsive Infantile Hemangiomas
- NOTCH pathway activation in infantile hemangiomas
- The expression of renin–angiotensin–aldosterone axis components in infantile hemangioma tissue and the impact of propranolol treatment
- Abnormal elastin and collagen deposition is present in extracranial arteriovenous malformations: A comparison to intracranial disease.
Showing 5 of 12 shared publications
- Elevated Expression of Matrix Metalloproteinase-9 not Matrix Metalloproteinase-2 Contributes to Progression of Extracranial Arteriovenous Malformation
- Expression of β-Adrenergic Receptor Subtypes in Proliferative, Involuted, and Propranolol-Responsive Infantile Hemangiomas
- NOTCH pathway activation in infantile hemangiomas
- The expression of renin–angiotensin–aldosterone axis components in infantile hemangioma tissue and the impact of propranolol treatment
- Abnormal elastin and collagen deposition is present in extracranial arteriovenous malformations: A comparison to intracranial disease.
Showing 5 of 8 shared publications
- NOTCH pathway activation in infantile hemangiomas
- Extracranial arteriovenous malformations demonstrate dysregulated TGF-β/BMP signaling and increased circulating TGF-β1
- Upregulated MicroRNA-21 Drives the Proliferation of Lymphatic Malformation Endothelial Cells by Inhibiting PDCD4
- Quantitative plasma proteomic analysis in children after superior cavopulmonary anastomosis with pulmonary arteriovenous malformations
- Mural Cells Initiate Endothelial-to-Mesenchymal Transition in Adjacent Endothelial Cells in Extracranial AVMs
Showing 5 of 8 shared publications
- NOTCH pathway activation in infantile hemangiomas
- Abnormal elastin and collagen deposition is present in extracranial arteriovenous malformations: A comparison to intracranial disease.
- Extracranial arteriovenous malformations demonstrate dysregulated TGF-β/BMP signaling and increased circulating TGF-β1
- Upregulated MicroRNA-21 Drives the Proliferation of Lymphatic Malformation Endothelial Cells by Inhibiting PDCD4
- Mural Cells Initiate Endothelial-to-Mesenchymal Transition in Adjacent Endothelial Cells in Extracranial AVMs
Showing 5 of 7 shared publications
- Upregulated MicroRNA-21 Drives the Proliferation of Lymphatic Malformation Endothelial Cells by Inhibiting PDCD4
- Mural Cells Initiate Endothelial-to-Mesenchymal Transition in Adjacent Endothelial Cells in Extracranial AVMs
- Rescue of Angiopoietin‐2 Inhibits Proliferation of Lymphatic Malformation Endothelial Cells
- M2 Macrophage Polarization Characterizes an Immunosuppressive Microenvironment in Extracranial Arteriovenous Malformations
- Upregulated MicroRNA-21 Drives the Proliferation of Lymphatic Malformation Endothelial Cells by Inhibiting PDCD4
- Quantitative plasma proteomic analysis in children after superior cavopulmonary anastomosis with pulmonary arteriovenous malformations
- Rescue of Angiopoietin‐2 Inhibits Proliferation of Lymphatic Malformation Endothelial Cells
- The expression of renin–angiotensin–aldosterone axis components in infantile hemangioma tissue and the impact of propranolol treatment
- Abnormal elastin and collagen deposition is present in extracranial arteriovenous malformations: A comparison to intracranial disease.
- Abnormal elastin and collagen deposition is present in extracranial arteriovenous malformations: A comparison to intracranial disease.
- Presence of estrogen and progesterone receptors in proliferating and involuting infantile hemangiomas
- NOTCH pathway activation in infantile hemangiomas
- Presence of estrogen and progesterone receptors in proliferating and involuting infantile hemangiomas
- Extracranial arteriovenous malformations demonstrate dysregulated TGF-β/BMP signaling and increased circulating TGF-β1
- Extracranial arteriovenous malformations demonstrate dysregulated TGF-β/BMP signaling and increased circulating TGF-β1
- Upregulated MicroRNA-21 Drives the Proliferation of Lymphatic Malformation Endothelial Cells by Inhibiting PDCD4
- Rescue of Angiopoietin‐2 Inhibits Proliferation of Lymphatic Malformation Endothelial Cells
- Upregulated MicroRNA-21 Drives the Proliferation of Lymphatic Malformation Endothelial Cells by Inhibiting PDCD4
- Rescue of Angiopoietin‐2 Inhibits Proliferation of Lymphatic Malformation Endothelial Cells
- Upregulated MicroRNA-21 Drives the Proliferation of Lymphatic Malformation Endothelial Cells by Inhibiting PDCD4
- Rescue of Angiopoietin‐2 Inhibits Proliferation of Lymphatic Malformation Endothelial Cells
- Upregulated MicroRNA-21 Drives the Proliferation of Lymphatic Malformation Endothelial Cells by Inhibiting PDCD4
- Rescue of Angiopoietin‐2 Inhibits Proliferation of Lymphatic Malformation Endothelial Cells
- Elevated Expression of Matrix Metalloproteinase-9 not Matrix Metalloproteinase-2 Contributes to Progression of Extracranial Arteriovenous Malformation
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