Haihong Zhang
Researcher
Also affiliated: Agency for Science, Technology and Research (2023); Fujian Medical University (2024–2026); Arkansas Children's Hospital (2016–2026); 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); Chinese General Hospital College of Nursing and Liberal Arts (2015); Fujian Women and Children Hospital (2024–2025); Qinghai University Affiliated Hospital (2024); Guangzhou Center for Disease Control and Prevention (2015); West China Hospital of Sichuan University (2023); Shanghai Children's Medical Center (2025–2026); People's Liberation Army No. 150 Hospital (2015); Lanzhou University Second Hospital (2024–2026); Beijing Chuiyangliu Hospital (2025); Tang Du Hospital (2019); Chinese People's Liberation Army (2015); Aviation General Hospital (2024); State Key Laboratory of Genetic Engineering (2019); Lanzhou University (2024–2026); Air Force Medical University (2019)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Haihong Zhang's research focuses on disease mechanisms and molecular biology. Her work includes investigating the role of overexpressed PKM2 in promoting macrophage phagocytosis and atherosclerosis, as detailed in a 2022 publication. She has also studied signaling pathways in extracranial arteriovenous malformations, specifically the dysregulation of TGF-β/BMP signaling and increased circulating TGF-β1, also in 2022. Another area of her research involves the impact of microRNA-21 on the proliferation of lymphatic malformation endothelial cells by inhibiting PDCD4, as published in 2023. Zhang's scholarship metrics include an h-index of 11, with a total of 48 publications and 440 citations. She has collaborated with several researchers at the University of Arkansas for Medical Sciences, including Gresham T. Richter (7 shared publications), Graham M. Strub (6 shared publications), Ravi W. Sun (4 shared publications), and Syed Hassan Mehdi (3 shared publications).
Metrics
- h-index: 11
- Publications: 50
- Citations: 448
Selected Publications
-
M2 Macrophage Polarization Characterizes an Immunosuppressive Microenvironment in Extracranial Arteriovenous Malformations (2026)
-
Rescue of Angiopoietin‐2 Inhibits Proliferation of Lymphatic Malformation Endothelial Cells (2025)
-
Mural Cells Initiate Endothelial-to-Mesenchymal Transition in Adjacent Endothelial Cells in Extracranial AVMs (2024)
-
Quantitative plasma proteomic analysis in children after superior cavopulmonary anastomosis with pulmonary arteriovenous malformations (2024)
-
Upregulated MicroRNA-21 Drives the Proliferation of Lymphatic Malformation Endothelial Cells by Inhibiting PDCD4 (2023)
-
Extracranial arteriovenous malformations demonstrate dysregulated TGF-β/BMP signaling and increased circulating TGF-β1 (2022)
-
Extracranial arteriovenous malformations demonstrate dysregulated TGF-β/BMP signaling and increased circulating TGF-β1 (2022)
-
Presence of estrogen and progesterone receptors in proliferating and involuting infantile hemangiomas (2021)
-
NOTCH pathway activation in infantile hemangiomas (2020)
-
Abnormal elastin and collagen deposition is present in extracranial arteriovenous malformations: A comparison to intracranial disease. (2019)
-
The expression of renin–angiotensin–aldosterone axis components in infantile hemangioma tissue and the impact of propranolol treatment (2017)
-
Expression of β-Adrenergic Receptor Subtypes in Proliferative, Involuted, and Propranolol-Responsive Infantile Hemangiomas (2016)
-
Elevated Expression of Matrix Metalloproteinase-9 not Matrix Metalloproteinase-2 Contributes to Progression of Extracranial Arteriovenous Malformation (2016)
Collaboration Network
Top Collaborators
- Extracranial arteriovenous malformations demonstrate dysregulated TGF-β/BMP signaling and increased circulating TGF-β1
- Presence of estrogen and progesterone receptors in proliferating and involuting infantile hemangiomas
- 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
- Extracranial arteriovenous malformations demonstrate dysregulated TGF-β/BMP signaling and increased circulating TGF-β1
Showing 5 of 7 shared publications
- 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
- Extracranial arteriovenous malformations demonstrate dysregulated TGF-β/BMP signaling and increased circulating TGF-β1
- Mural Cells Initiate Endothelial-to-Mesenchymal Transition in Adjacent Endothelial Cells in Extracranial AVMs
Showing 5 of 6 shared publications
- 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
- Rescue of Angiopoietin‐2 Inhibits Proliferation of Lymphatic Malformation Endothelial Cells
- Extracranial arteriovenous malformations demonstrate dysregulated TGF-β/BMP signaling and increased circulating TGF-β1
- 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
- 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
- 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
- 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
- Presence of estrogen and progesterone receptors in proliferating and involuting infantile hemangiomas
- Presence of estrogen and progesterone receptors in proliferating and involuting 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
Similar Researchers
Based on overlapping research topics