Carol Morris
Researcher
Also affiliated: University of Technology Sydney (2009); Northeastern Oklahoma A&M College (1985); Memorial Sloan Kettering Cancer Center (2024); The University of Queensland (2011); University of New Mexico (1992–1998); Wayne State University (2002); UNSW Sydney (1996–2009); Yale University (1988–1990); University of Florida (1987–1988); University of New Haven (1988); University of Colorado Health (2000); Alibaba Group (United States) (2002); Vision Cooperative Research Centre (1996–2009); Prince of Wales Hospital (1993–1994); VA Connecticut Research and Education Foundation (1988); Faculty of 1000 (United States) (1989); BioInVision (United States) (2017–2018); Smith-Kettlewell Eye Research Institute (2009); Saint Louis University (1975); Southern Cross University (2006–2012); University of Sheffield (1993)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Carol Morris's research focuses on understanding the mechanisms of disease, particularly in the context of retinal ischemic injury and multiple myeloma bone disease. She has investigated the role of myeloid cells and specific molecular pathways, such as the arginase 1/ornithine decarboxylase pathway and HDAC3, in modulating inflammatory responses and promoting tissue repair in the retina. Her work includes the development and characterization of animal models, as demonstrated by her publications on improved animal models of multiple myeloma bone disease and multi-color flow cytometry protocols for analyzing myeloid cells in mouse retinas.
Morris has also explored proteomic analyses of ocular fluids, such as aqueous humor, to identify novel insights into the pathophysiology of retinal vascular occlusive diseases. Her scholarship metrics include an h-index of 25, 78 total publications, and over 2,000 total citations, designating her as a highly cited researcher. She actively collaborates with researchers at the University of Arkansas for Medical Sciences, including Abdelrahman Y. Fouda, Esraa Shosha, Rami Ahmad Shahror, and Nancy J. Rusch, with whom she shares multiple publications.
Metrics
- h-index: 25
- Publications: 78
- Citations: 2,034
Selected Publications
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Myeloid HDAC3 deletion protects against traumatic optic injury (2026)
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HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis (2025)
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The role of efferocytosis in ischemic stroke and insights from retinopathy (2025)
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Disrupting the CD47/SIRPα Axis Protects Against Traumatic Optic Neuropathy (2025)
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Disrupting the CD47/SIRPα Axis as a Novel and Translational Therapy for Stroke (Abstract ID: 161422) (2025)
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Proteomic Analysis of Aqueous Humor in Central Retinal Artery Occlusion: Unveiling Novel Insights Into Disease Pathophysiology (2024)
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Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury (2024)
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Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions (2024)
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The arginase 1/ornithine decarboxylase pathway suppresses HDAC3 to ameliorate the myeloid cell inflammatory response: implications for retinal ischemic injury (2023)
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Multi-color Flow Cytometry Protocol to Characterize Myeloid Cells in Mouse Retina Research (2023)
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Herbal Extracts from Lycii Radicis Corex and Achyranthes japonica Prevent Multiple Myeloma (2021)
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An Improved Animal Model of Multiple Myeloma Bone Disease (2021)
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Animal Models of Multiple Myeloma Bone Disease (2021)
Collaboration Network
Top Collaborators
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions
- The arginase 1/ornithine decarboxylase pathway suppresses HDAC3 to ameliorate the myeloid cell inflammatory response: implications for retinal ischemic injury
- Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury
- Multi-color Flow Cytometry Protocol to Characterize Myeloid Cells in Mouse Retina Research
- Proteomic Analysis of Aqueous Humor in Central Retinal Artery Occlusion: Unveiling Novel Insights Into Disease Pathophysiology
Showing 5 of 10 shared publications
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions
- The arginase 1/ornithine decarboxylase pathway suppresses HDAC3 to ameliorate the myeloid cell inflammatory response: implications for retinal ischemic injury
- Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury
- Multi-color Flow Cytometry Protocol to Characterize Myeloid Cells in Mouse Retina Research
- Proteomic Analysis of Aqueous Humor in Central Retinal Artery Occlusion: Unveiling Novel Insights Into Disease Pathophysiology
Showing 5 of 7 shared publications
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions
- The arginase 1/ornithine decarboxylase pathway suppresses HDAC3 to ameliorate the myeloid cell inflammatory response: implications for retinal ischemic injury
- Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury
- Proteomic Analysis of Aqueous Humor in Central Retinal Artery Occlusion: Unveiling Novel Insights Into Disease Pathophysiology
- Disrupting the CD47/SIRPα Axis as a Novel and Translational Therapy for Stroke (Abstract ID: 161422)
Showing 5 of 7 shared publications
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions
- The arginase 1/ornithine decarboxylase pathway suppresses HDAC3 to ameliorate the myeloid cell inflammatory response: implications for retinal ischemic injury
- Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury
- The role of efferocytosis in ischemic stroke and insights from retinopathy
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions
- Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury
- Proteomic Analysis of Aqueous Humor in Central Retinal Artery Occlusion: Unveiling Novel Insights Into Disease Pathophysiology
- Disrupting the CD47/SIRPα Axis Protects Against Traumatic Optic Neuropathy
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- Animal Models of Multiple Myeloma Bone Disease
- An Improved Animal Model of Multiple Myeloma Bone Disease
- Herbal Extracts from Lycii Radicis Corex and Achyranthes japonica Prevent Multiple Myeloma
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions
- Proteomic Analysis of Aqueous Humor in Central Retinal Artery Occlusion: Unveiling Novel Insights Into Disease Pathophysiology
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- Animal Models of Multiple Myeloma Bone Disease
- An Improved Animal Model of Multiple Myeloma Bone Disease
- Animal Models of Multiple Myeloma Bone Disease
- Herbal Extracts from Lycii Radicis Corex and Achyranthes japonica Prevent Multiple Myeloma
- The arginase 1/ornithine decarboxylase pathway suppresses HDAC3 to ameliorate the myeloid cell inflammatory response: implications for retinal ischemic injury
- Multi-color Flow Cytometry Protocol to Characterize Myeloid Cells in Mouse Retina Research
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions
- Proteomic Analysis of Aqueous Humor in Central Retinal Artery Occlusion: Unveiling Novel Insights Into Disease Pathophysiology
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions
- Proteomic Analysis of Aqueous Humor in Central Retinal Artery Occlusion: Unveiling Novel Insights Into Disease Pathophysiology
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- Myeloid HDAC3 deletion protects against traumatic optic injury
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- Myeloid HDAC3 deletion protects against traumatic optic injury
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