Esraa Shosha
Assistant Professor
Also affiliated: Cairo University (2019–2026); Benha University (2021); Augusta University (2014–2021); Discovery Institute (2015–2021); Charlie Norwood VA Medical Center (2016–2021); Veterans Health Administration (2016); Augusta University Health (2016–2022); Georgia Regents Medical Center (2015–2016)
Faculty Researcher
COM | Pharmacology Channel & Hypertension
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Esraa Shosha investigates the mechanisms underlying retinal ischemia/reperfusion injury, with a particular focus on the role of arginase enzymes and myeloid cells. Her research has explored how endothelial arginase 2 contributes to mitochondrial dysfunction in the retina during ischemic events. Shosha also studies how arginase 1 can limit abnormal blood vessel growth (neovascularization) in the retina and promote repair. Her work has examined the inflammatory response in myeloid cells and its connection to retinal ischemic injury, including the interplay between the arginase 1/ornithine decarboxylase pathway and inflammatory mediators like HDAC3.
Further research by Shosha has delved into metabolic function in models of diabetes, specifically investigating retinal metabolic function in Akita mice with Type 1 diabetes. She has also explored the potential therapeutic applications of pegylated arginase 1 for treating injuries in both the retina and brain. Shosha collaborates with researchers at the University of Arkansas for Medical Sciences, including Abdelrahman Y. Fouda, Carol Morris, Nancy J. Rusch, and Rami Ahmad Shahror. Her scholarship metrics include an h-index of 15, with 48 total publications and 671 total citations.
Metrics
- h-index: 15
- Publications: 48
- Citations: 686
Selected Publications
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CD5L promotes efferocytosis and resolution of retinal ischemic injury (2026)
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A metabolic switch in retinal angiogenesis: Histone deacetylase 3 (2026)
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Systemic Lactate Dehydrogenase Levels as a Predictor of Progression from Non-Proliferative to Proliferative Diabetic Retinopathy (2025)
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HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis (2025)
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HDAC3 Drives Retinal Endothelial Cell Angiogenesis: Potential Therapeutic Implications for Retinopathy (Abstract ID: 161164) (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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Efferocytosis and retinal clean-up: Role of histone deacetylase 3 in ischemic retinopathy (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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Targeting proliferative retinopathy: Arginase 1 limits vitreoretinal neovascularization and promotes angiogenic repair (2022)
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Investigation of Retinal Metabolic Function in Type 1 Diabetic Akita Mice (2022)
Grants & Funding
As listed on this researcher's institutional profile.
- Role of endothelial HDAC3 in proliferative retinopathy American Heart Association Principal Investigator
Collaboration Network
Top Collaborators
- Targeting proliferative retinopathy: Arginase 1 limits vitreoretinal neovascularization and promotes angiogenic repair
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions
- Investigation of Retinal Metabolic Function in Type 1 Diabetic Akita Mice
- 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
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
- 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)
- 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
- Targeting proliferative retinopathy: Arginase 1 limits vitreoretinal neovascularization and promotes angiogenic repair
- Investigation of Retinal Metabolic Function in Type 1 Diabetic Akita Mice
- The arginase 1/ornithine decarboxylase pathway suppresses HDAC3 to ameliorate the myeloid cell inflammatory response: implications for retinal ischemic injury
- Targeting proliferative retinopathy: Arginase 1 limits vitreoretinal neovascularization and promotes angiogenic repair
- Investigation of Retinal Metabolic Function in Type 1 Diabetic Akita Mice
- The arginase 1/ornithine decarboxylase pathway suppresses HDAC3 to ameliorate the myeloid cell inflammatory response: implications for retinal ischemic injury
- 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
- 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
- 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 Drives Retinal Endothelial Cell Angiogenesis: Potential Therapeutic Implications for Retinopathy (Abstract ID: 161164)
- Targeting proliferative retinopathy: Arginase 1 limits vitreoretinal neovascularization and promotes angiogenic repair
- Investigation of Retinal Metabolic Function in Type 1 Diabetic Akita Mice
- Targeting proliferative retinopathy: Arginase 1 limits vitreoretinal neovascularization and promotes angiogenic repair
- Investigation of Retinal Metabolic Function in Type 1 Diabetic Akita Mice
- Targeting proliferative retinopathy: Arginase 1 limits vitreoretinal neovascularization and promotes angiogenic repair
- Investigation of Retinal Metabolic Function in Type 1 Diabetic Akita Mice
- Targeting proliferative retinopathy: Arginase 1 limits vitreoretinal neovascularization and promotes angiogenic repair
- Investigation of Retinal Metabolic Function in Type 1 Diabetic Akita Mice
- 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
- Proteomic Analysis of Aqueous Humor in Central Retinal Artery Occlusion: Unveiling Novel Insights Into Disease Pathophysiology
- Systemic Lactate Dehydrogenase Levels as a Predictor of Progression from Non-Proliferative to Proliferative Diabetic Retinopathy
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