Nancy J. Rusch
Distinguished Professor
Also affiliated: Broad Institute (2014); University of Vermont (2010); University of Iowa (1985–2008); American Heart Association (2002); Mayo Clinic (1983–1988); University of Nevada, Reno (1987); Providence Regional Medical Center Everett (1989); Innsbruck Medical University (1997–1998); University of Antwerp (2008); Université de Bordeaux (2002); Inserm (2002); Oregon Health & Science University (1989); Wisconsin Lutheran College (1992); Baylor College of Medicine (2007); Medical College of Wisconsin (1988–2005); Max Delbrück Center (2014); Providence Portland Medical Center (1989); The University of Kansas Cancer Center (2014); Milwaukee VA Medical Center (1996–2004); Weill Cornell Medical College in Qatar (2010); Ingénierie Moléculaire et Physiopathologie Articulaire (2002); Czech Academy of Sciences, Institute of Physiology (1995); Rusk Rehabilitation (1981); Laboratoire de Physiologie Cellulaire (2002); University of Rochester (2012); University of Cincinnati (1987); Graduate School USA (1995)
Faculty Researcher
College of Medicine
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Nancy J. Rusch's research focuses on the mechanisms underlying vascular and tissue health, with a particular emphasis on the roles of myeloid cells, endothelial cells, and specific signaling pathways in disease states. Her work has investigated the impact of factors such as PCSK9 on efferocytosis in endothelial cells and the promotion of vascular aging. Rusch has also explored the involvement of myeloid cells in ischemic retinopathies and the therapeutic potential of targeting pathways like the arginase 1/ornithine decarboxylase pathway to suppress inflammation and ameliorate retinal ischemic injury.
Her laboratory has also examined drug-induced lymphostasis, specifically the effects of doxorubicin on the rat mesenteric circulation, and has explored potential preventative strategies using agents like dantrolene. Rusch's research group investigates how cellular processes, including epigenetic regulation and signaling cascades, contribute to conditions such as hepatocellular carcinoma and vascular aging. Her scholarship is supported by a significant publication record, with 195 total publications and an h-index of 42. She has established collaborations with researchers at the University of Arkansas for Medical Sciences, including Abdelrahman Y. Fouda, Shengyu Mu, Amanda J. Stolarz, and Esraa Shosha, with whom she shares multiple co-authored publications.
Metrics
- h-index: 42
- Publications: 197
- Citations: 5,036
Selected Publications
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Heat shock protein 72 is a druggable target during cold storage to improve graft outcome after kidney transplantation (2026)
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CD5L promotes efferocytosis and resolution of retinal ischemic injury (2026)
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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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Smooth muscle excitability (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)
Grants & Funding
As listed on this researcher's institutional profile.
- 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
- Vascular Calcium Channel Expression in Hypertension NIH Principal Investigator
- PSD95 scaffolding of vascular K+ channels in hypertension NIH Co-Investigator
- Expanding Translational Research in Arkansas NIH Co-Investigator
- Doxorubicin suppression of lymphatic function and therapeutic reversal NIH Principal Investigator
- REGULATION OF VENOUS MUSCLE K+ CHANNELS NIH Principal Investigator
- J. NRSA Training NIH Principal Investigator
- TROPHIC EFFECT OF SYMPATHETIC NERVES ON ARTERIAL MUSCLE NIH Principal Investigator
- Calcium Channels in Neonatal Pulmonary Hypertension NIH Principal Investigator
- Center for Studies of Host Response to Cancer Therapy NIH Co-Investigator
- Dr. Rusch Start Up Account UAMS College of Medicine Principal Investigator
- VASCULAR MUSCLE CALCIUM CURRENTS IN HYPERTENSION NIH Principal Investigator
- Connect Arkansas Research Scholars (CARS) Program University of Arkansas at Pine Bluff 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
- 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
- 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
- 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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