Nancy J. Rusch
Distinguished Professor
faculty
College of Medicine
Research Areas
Biography and Research Information
OverviewAI-generated summary
Nancy J. Rusch, Distinguished Professor in the College of Medicine at the University of Arkansas for Medical Sciences, studies the role of myeloid cells in various disease states, including ischemic retinopathies and vascular aging. Her research investigates how these cells, particularly macrophages, influence disease progression and potential therapeutic interventions.
Recent work by Rusch and her collaborators has focused on the mechanisms by which myeloid cell function impacts inflammatory responses and tissue injury. This includes exploring pathways involving histone deacetylase 3 (HDAC3) and the arginase 1/ornithine decarboxylase pathway in the context of retinal ischemic injury. Her group also examines the role of endothelial cells in mediating inflammatory processes and their potential macrophage-like functions.
Further research interests include the mechanisms underlying drug-induced lymphedema and potential therapeutic strategies, as demonstrated by studies on dantrolene's effects in preventing doxorubicin-induced lymphostasis. Rusch also investigates the complex signaling pathways involved in conditions such as hepatocellular carcinoma, exploring epigenetic dysregulation and its impact on cellular signaling. Her scholarship metrics include an h-index of 42, 192 total publications, and 4,950 total citations.
Metrics
- h-index: 42
- Publications: 194
- Citations: 5,000
Selected Publications
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Nanoencapsulated gamma-oryzanol enhances fibroblast proliferation, migration, and reduces oxidative stress in H2O2-induced cellular aging model (2025)
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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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Rhythmic Contractions of Lymph Vessels and Lymph Flow Are Disrupted in Hypertensive Rats (2024)
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Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury (2024)
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The Loss of an Orphan Nuclear Receptor NR2E3 Augments Wnt/β‐catenin Signaling via Epigenetic Dysregulation that Enhances Sp1‐β catenin‐p300 Interactions in Hepatocellular Carcinoma (2024)
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SS-31 Attenuates Doxorubicin-induced Cardiomyoblast H9C2 Cell Senescence (2024)
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Abstract 3011: The loss of an orphan nuclear receptor NR2E3 augments Wnt/β-Catenin signaling via epigenetic dysregulation that links to the Sp1-β catenin-p300 interactions in hepatocellular carcinoma (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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PCSK9 attenuates efferocytosis in endothelial cells and promotes vascular aging (2023)
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Mitochondrial proton leak in cardiac aging (2023)
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Opinion: Endothelial Cells - Macrophage-Like Gatekeepers? (2022)
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Drug-Related Lymphedema: Mysteries, Mechanisms, and Potential Therapies (2022)
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Dantrolene Prevents the Lymphostasis Caused by Doxorubicin in the Rat Mesenteric Circulation (2021)
Grants & Funding
- MicroRNA to decrease vascular CaV1.2 in hypertension NIH Co-Investigator
- AHA-Vascular TRPC3 Channels as Antihypertensive Targets American Heart Association (SouthWest Affiliate) Principal Investigator
- Beta adrenergic receptor-mediated vasodilation of cerebral collateral arteries- Resubmission- Resubmission American Heart Association Principal Investigator
- T32 Campus Match funding Account UAMS College of Medicine Principal Investigator
- Pharmacology Dept GEF Account UAMS College of Medicine Principal Investigator
- Long-term Antihypertensive Therapy by Delivery of the BK Channel Gene to VSMCs NIH Principal Investigator
- Role of mitoBK channels in rat renal cold preservation American Heart Association (SouthWest Affiliate) Principal Investigator
- Role of Cerebrovascular K+ Channels in Hypertension NIH Principal Investigator
Collaboration Network
Top Collaborators
- Drug-Related Lymphedema: Mysteries, Mechanisms, and Potential Therapies
- Dantrolene Prevents the Lymphostasis Caused by Doxorubicin in the Rat Mesenteric Circulation
- Opinion: Endothelial Cells - Macrophage-Like Gatekeepers?
- Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury
- Mitochondrial proton leak in cardiac aging
Showing 5 of 7 shared publications
- PCSK9 attenuates efferocytosis in endothelial cells and promotes vascular aging
- Drug-Related Lymphedema: Mysteries, Mechanisms, and Potential Therapies
- Dantrolene Prevents the Lymphostasis Caused by Doxorubicin in the Rat Mesenteric Circulation
- Opinion: Endothelial Cells - Macrophage-Like Gatekeepers?
- Rhythmic Contractions of Lymph Vessels and Lymph Flow Are Disrupted in Hypertensive Rats
Showing 5 of 6 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
- Opinion: Endothelial Cells - Macrophage-Like Gatekeepers?
- Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury
- The role of efferocytosis in ischemic stroke and insights from retinopathy
Showing 5 of 6 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
- 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
- PCSK9 attenuates efferocytosis in endothelial cells and promotes vascular aging
- Opinion: Endothelial Cells - Macrophage-Like Gatekeepers?
- Mitochondrial proton leak in cardiac aging
- SS-31 Attenuates Doxorubicin-induced Cardiomyoblast H9C2 Cell Senescence
- Drug-Related Lymphedema: Mysteries, Mechanisms, and Potential Therapies
- Dantrolene Prevents the Lymphostasis Caused by Doxorubicin in the Rat Mesenteric Circulation
- Rhythmic Contractions of Lymph Vessels and Lymph Flow Are Disrupted in Hypertensive Rats
- Mitochondrial proton leak in cardiac aging
- SS-31 Attenuates Doxorubicin-induced Cardiomyoblast H9C2 Cell Senescence
- Nanoencapsulated gamma-oryzanol enhances fibroblast proliferation, migration, and reduces oxidative stress in H2O2-induced cellular aging model
- 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
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- PCSK9 attenuates efferocytosis in endothelial cells and promotes vascular aging
- Opinion: Endothelial Cells - Macrophage-Like Gatekeepers?
- Mitochondrial proton leak in cardiac aging
- SS-31 Attenuates Doxorubicin-induced Cardiomyoblast H9C2 Cell Senescence
- Mitochondrial proton leak in cardiac aging
- SS-31 Attenuates Doxorubicin-induced Cardiomyoblast H9C2 Cell Senescence
- PCSK9 attenuates efferocytosis in endothelial cells and promotes vascular aging
- Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
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