A. J. Cunningham
Researcher
Also affiliated: Ontario Institute for Cancer Research (1978–2004); Australian National University (1965–1977); Royal College of Surgeons in Ireland (1988–2001); University of Ottawa (1984); University of Toronto (1978–2004); Universität Ulm (2002); Cappagh National Orthopaedic Hospital (2001); University Hospital of Wales (2017); Cancer Institute (WIA) (1978); Beaumont Hospital (1988–2007); The Alfred Hospital (2014); Botsford Hospital (2007); Cork University Hospital (1992–2001); Princess Margaret Cancer Centre (1995–2001); Northern Health and Social Care Trust (2025); In-Q-Tel (2003); The Catholic University of Korea St. Vincent's Hospital (1985); St. Vincent's University Hospital (1985); Beaumont Hospital, Dearborn (2007); National Maternity Hospital (1989); Institute for Cancer Prevention (2002); University of Sunderland (2010–2012)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
A. J. Cunningham's research interests encompass several areas, including the mechanisms of myeloid HDAC3 deletion in protecting against traumatic optic injury and its role in retinal endothelial cell metabolic reprogramming and angiogenesis. Cunningham's work has been supported by various grants, and they have published extensively in peer-reviewed journals. Their scholarship metrics include an h-index of 14, with a total of 65 publications and 1,499 citations. Cunningham has collaborated with researchers at the University of Arkansas for Medical Sciences, including Abdelrahman Y. Fouda, Carol Morris, and Piyanan Chuesiang, with whom they share multiple publications.
Metrics
- h-index: 14
- Publications: 65
- Citations: 1,501
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)
Collaboration Network
Top Collaborators
- 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
- 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
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- Myeloid HDAC3 deletion protects against traumatic optic injury
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