R
Rami Ahmad Shahror
Researcher
faculty
Pharmacology & Toxicology, College of Medicine
10 h-index
25 pubs
436 cited
Research Areas
Biography and Research Information
OverviewAI-generated summary
Rami Ahmad Shahror's research focuses on the role of myeloid cells and innate immune responses in central nervous system and ocular diseases. His work investigates mechanisms underlying neuroinflammation and its contribution to conditions such as traumatic brain injury and ischemic retinopathies. Shahror's publications explore the modulation of inflammatory pathways, including the arginase 1/ornithine decarboxylase pathway and the role of HDAC3 in myeloid cell function, to ameliorate injury in retinal ischemic models. He also examines the potential of nanosystems for ocular drug delivery and employs techniques like multi-color flow cytometry to characterize myeloid cell populations in mouse retina research. Shahror has 25 publications with 424 citations and an h-index of 10. He collaborates with researchers at the University of Arkansas for Medical Sciences, including Abdelrahman Y. Fouda, Carol Morris, Esraa Shosha, and Melissa Wild.
Metrics
- h-index: 10
- Publications: 25
- Citations: 436
Selected Publications
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CD5L promotes efferocytosis and resolution of retinal ischemic injury (2026)
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Recent advances and future challenges in nanosystems for ocular drug delivery (2025)
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Myeloid HDAC3 Deletion Protects Against Traumatic Optic Injury (2025)
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Disrupting the CD47/SIRPα Axis Protects Against Traumatic Optic Neuropathy (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)
Collaboration Network
Top Collaborators
Abdelrahman Y. Fouda
University of Arkansas for Medical Sciences
8 shared publications
In database
- 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 8 shared publications
Carol Morris
University of Arkansas for Medical Sciences
6 shared publications
In database
- 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 6 shared publications
Esraa Shosha
University of Arkansas for Medical Sciences
4 shared publications
In database
- 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
Melissa Wild
University of Arkansas for Medical Sciences
4 shared publications
In database
- 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
Junyun He
University of Maryland, Baltimore (US)
3 shared publications
- Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with inflammatory neurodegeneration
- Brain innate immune response via miRNA-TLR7 sensing in polymicrobial sepsis
- Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with hyperphagocytosis and inflammatory neurodegeneration
Yun Li
University of Maryland, Baltimore (US)
3 shared publications
- Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with inflammatory neurodegeneration
- Brain innate immune response via miRNA-TLR7 sensing in polymicrobial sepsis
- Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with hyperphagocytosis and inflammatory neurodegeneration
Junfang Wu
University of Maryland, Baltimore (US)
3 shared publications
- Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with inflammatory neurodegeneration
- Brain innate immune response via miRNA-TLR7 sensing in polymicrobial sepsis
- Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with hyperphagocytosis and inflammatory neurodegeneration
Nancy J. Rusch
University of Arkansas for Medical Sciences
3 shared publications
In database
- 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
Rodney M. Ritzel
University of Maryland, Baltimore (US)
2 shared publications
- Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with inflammatory neurodegeneration
- Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with hyperphagocytosis and inflammatory neurodegeneration
Yun Jiao
University of Maryland, Baltimore (US)
2 shared publications
- Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with inflammatory neurodegeneration
- Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with hyperphagocytosis and inflammatory neurodegeneration
Zhuofan Lei
University of Maryland, Baltimore (US)
2 shared publications
- Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with inflammatory neurodegeneration
- Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with hyperphagocytosis and inflammatory neurodegeneration
Sarah J. Doran
University of Maryland, Baltimore (US)
2 shared publications
- Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with inflammatory neurodegeneration
- Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with hyperphagocytosis and inflammatory neurodegeneration
Rebecca J. Henry
University of Maryland, Baltimore (US)
2 shared publications
- Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with inflammatory neurodegeneration
- Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with hyperphagocytosis and inflammatory neurodegeneration
Shaolin Liu
Howard University (US)
2 shared publications
- Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with inflammatory neurodegeneration
- Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with hyperphagocytosis and inflammatory neurodegeneration
Bogdan A. Stoica
University of Maryland, Baltimore (US)
2 shared publications
- Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with inflammatory neurodegeneration
- Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with hyperphagocytosis and inflammatory neurodegeneration
Similar Researchers
Based on overlapping research topics
Aya A Mohammed
University of Arkansas for Medical Sciences
Immune Response and Inflammation
Retinal Diseases and Treatments
Nanoparticles: synthesis and applications
Sara M. Venier
University of Arkansas at Fayetteville
Immune Response and Inflammation
Neuroscience and Neuropharmacology Research
Traumatic Brain Injury Research
Melissa Wild
University of Arkansas for Medical Sciences
Neuroscience and Neuropharmacology Research
Retinal Diseases and Treatments
Disease Mechanisms Research
Andreea M. Bujor
University of Arkansas for Medical Sciences
Immune Response and Inflammation
Disease Mechanisms Research
Molecular Biology Techniques and Applications
Carol Morris
University of Arkansas for Medical Sciences
Immune Response and Inflammation
Retinal Diseases and Treatments
Disease Mechanisms Research
Esraa Shosha
University of Arkansas for Medical Sciences
Immune Response and Inflammation
Neuroscience and Neuropharmacology Research
Retinal Diseases and Treatments