Rami Ahmad Shahror

Rami Ahmad Shahror, M.Sc., M.Med.Sc., Ph.D.

UAMS

Also affiliated: University of Maryland, Baltimore (2020–2023); National Health Research Institutes (2019–2020); Örebro University (2015–2018); University of Arkansas Medical Center (2024); Taipei Medical University (2019–2020)

Pharmacology & Toxicology, College of Medicine

11 h-index 27 pubs 473 cited

Research Areas

Biomedical Subjects

Links

ORCID Lab Website Research Group UAMS TRI Profile

OverviewAI-generated summary

Rami Ahmad Shahror's research focuses on understanding the mechanisms of central nervous system and retinal injuries, particularly in the context of traumatic brain injury (TBI) and ischemic retinopathies. He investigates the role of innate immune responses, specifically microglial and myeloid cell activation, in disease progression and potential therapeutic interventions. Shahror has studied the use of mesenchymal stem cells (MSCs), including genetically modified MSCs overexpressing Fibroblast Growth Factor 21, as a treatment strategy for TBI, examining their ability to promote cognitive recovery and neurogenesis. His work also explores the molecular pathways involved in inflammation and cell efferocytosis, such as the arginase 1/ornithine decarboxylase pathway and the role of HDAC3 in ameliorating inflammatory responses in retinal ischemic injury. Shahror's research utilizes mouse models and involves collaborations with researchers at the University of Arkansas for Medical Sciences. He has published 26 papers, accumulating 468 citations, with an h-index of 10.

Metrics

h-index: 11
Publications: 27
Citations: 473

Positions

Rami Ahmad Shahror, M.Sc., M.Med.Sc., Ph.D. publications 2023–2026

University of Arkansas for Medical Sciences Institution web page

Selected Publications

Temporal and Age-Dependent Regulation of Phagocytosis-Related Signatures After Ischemic Stroke: Cross-Species Transcriptomic Evidence (2026)

bioRxiv (Cold Spring Harbor Laboratory) DOI OpenAlex
CD5L promotes efferocytosis and resolution of retinal ischemic injury (2026)

Cell Death and Disease DOI OpenAlex
Myeloid HDAC3 deletion protects against traumatic optic injury (2026)

Cell Death Discovery DOI OpenAlex
Recent advances and future challenges in nanosystems for ocular drug delivery (2025)

Journal of Pharmacology and Experimental Therapeutics 10 citations DOI OpenAlex
Myeloid HDAC3 Deletion Protects Against Traumatic Optic Injury (2025)

Research Square DOI OpenAlex
Disrupting the CD47/SIRPα Axis Protects Against Traumatic Optic Neuropathy (2025)

Research Square DOI OpenAlex
Proteomic Analysis of Aqueous Humor in Central Retinal Artery Occlusion: Unveiling Novel Insights Into Disease Pathophysiology (2024)

Translational Vision Science & Technology 3 citations DOI OpenAlex
Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury (2024)

Journal of Neuroinflammation 17 citations DOI OpenAlex
Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions (2024)

Journal of Neuroinflammation 45 citations DOI OpenAlex
The arginase 1/ornithine decarboxylase pathway suppresses HDAC3 to ameliorate the myeloid cell inflammatory response: implications for retinal ischemic injury (2023)

Cell Death and Disease 28 citations DOI OpenAlex
Multi-color Flow Cytometry Protocol to Characterize Myeloid Cells in Mouse Retina Research (2023)

BIO-PROTOCOL 6 citations DOI OpenAlex