Edward T.H. Yeh
Chairman
Also affiliated: Scripps Research Institute (1997); Brigham and Women's Hospital (2013–2015); Grady Memorial Hospital (2006); Arthritis Foundation (1990); St. Luke's Episcopal Hospital (1998–2015); The University of Texas MD Anderson Cancer Center (2000–2023); Harvard University (1986–2015); University of Miami (1999); The University of Texas System (2003); Duke University (1994); Baylor College of Medicine (1995–2016); China Medical University (2011); University of Toronto (2004); University of Campania "Luigi Vanvitelli" (2007–2013); University of Arkansas Medical Center (2022–2025); University of Missouri Hospital (2018); University of Rochester Medicine (2013); Massachusetts General Hospital (1989–2015); Mount Sinai Medical Center (1999); Dana-Farber Cancer Institute (2013); Temple University Health System (2013); China Medical University Hospital (2011); National Taiwan University Hospital (2013); Brown Foundation (2006–2007); Ospedale Monaldi (2011); Institute of Molecular Medicine (1997); Dana-Farber Brigham Cancer Center (2013); Elsevier BV (Netherlands) (2008); Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases (1998–2007); University of Houston (2012); Taipei Medical University (2013); University of Rochester (2013); University of Missouri (2016–2022); University of Pennsylvania (2013); Temple University (2013); Texas A&M University (2004); The University of Texas Health Science Center at Houston (1993–2011)
Department Chairs, College of Medicine
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Edward T.H. Yeh's research group at the University of Arkansas for Medical Sciences focuses on the molecular mechanisms underlying cardiovascular complications associated with cancer therapies. His work has investigated the cardiotoxicity induced by agents such as doxorubicin and anthracyclines, as well as radiation-related heart disease. Yeh has also explored the role of C-reactive protein in cardiovascular health, specifically its proinflammatory effects on human endothelial cells and the modulation of these effects by anti-atherosclerosis drugs.
His publications include studies on the molecular basis of doxorubicin-induced cardiotoxicity and the prevention of anthracycline-induced cardiotoxicity. Yeh has also contributed to the understanding of cardiovascular complications of cancer therapy and radiation-related heart disease. He holds a high-impact researcher designation and is a member of the ARA Academy.
Yeh leads a research group and has collaborated with researchers at the University of Arkansas for Medical Sciences, including Hui‐Ming Chang on 12 shared publications. His scholarship metrics include an h-index of 88, 278 total publications, and over 29,000 total citations.
Metrics
- h-index: 85
- Publications: 264
- Citations: 28,541
Positions
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Distinguished Professor 2020–presentUniversity of Arkansas for Medical Sciences Internal Medicine ORCID
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Chairman publications 1992–2026University of Arkansas for Medical Sciences Department Chairs, College of Medicine Institutional directory
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Chairman 2016–2020University of Missouri Columbia Medicine ORCID
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Professor and Chair 2000–2016The University of Texas MD Anderson Cancer Center Cardiology ORCID
Selected Publications
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PP4 modulates macrophage-neutrophil crosstalk to restrict CCL5 -driven NETosis in sepsis (2026)
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Prevention of Heart Failure Induced by Doxorubicin with Early Administration of Dexrazoxane (PHOENIX Study): dose response and time course of dexrazoxane-induced degradation of topoisomerase 2b (2025)
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CYLD links the TRAF6/sNASP axis to TLR4 signaling in sepsis-induced acute lung injury (2025)
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Microglia‐Mediated Synaptic Dysfunction Contributes to Chemotherapy‐Related Cognitive Impairment (2025)
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Abstract 12348: Targeted Degradation of Topoisomerase 2b by Dexrazoxane for Prevention of Doxorubicin-Induced Cardiotoxicity: Dose and Time Course Study in Human (2023)
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Lactate: an intracellular metabolite regulates cell cycle progression (2023)
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Corticotropin-releasing hormone neurons in the central nucleus of amygdala are required for chronic stress-induced hypertension (2023)
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Promises and challenges of machine learning for device therapy in heart failure (2023)
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Dipeptidylpeptidase 4 promotes survival and stemness of acute myeloid leukemia stem cells (2023)
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Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation in mice (2022)
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Signaling pathways involved in NMDA ‐induced suppression of M‐channels in corticotropin‐releasing hormone neurons in central amygdala (2022)
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Dependence of Acute Myeloid Leukemia Development on Membrane Protein Dipeptidyl Peptidase 4 (2022)
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PEP-sNASP Peptide Alleviates LPS-Induced Acute Lung Injury Through the TLR4/TRAF6 Axis (2022)
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Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation (2022)
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Abstract 9710: Prevention of Doxorubicin-Induced Cardiotoxicity Through Targeted Degradation of Topoisomerase 2b (2021)
ARA Academy 2021 ARA Scholar
Dr. Yeh's research focuses on preventative treatment for anthracycline-induced cardiotoxicity. He earned his B.S. from UC Berkeley and M.D. from UC Davis, completing postdoctoral training under Nobel Laureate Baruj Benacerraf at Harvard. He founded Cardiology at MD Anderson Cancer Center and at the University of Missouri-Columbia improved the department's NIH research ranking from 98th to 76th nationally within three years.
Policy Impact
Recruited to UAMS from MD Anderson Cancer Center. Previously improved a department's NIH ranking from 98th to 76th nationally within three years.
Growth Areas
['Population Health Innovations & Clinical Research']
Grants & Funding
As listed on this researcher's institutional profile.
- Doxorubicin-induced Cardiotoxicity: The Role of Topoisomerase 2b NIH/Nat. Heart, Lung & Blood Institute Principal Investigator
- PATHOBIOCHEMISTRY OF ACUTE PROMYELOCYTIC LEUKEMIA NIH Principal Investigator
- Prevention of Heart Failure induced by Doxorubicin with Early Administration of Dexrazoxane NIH/Nat. Heart, Lung & Blood Institute Co-Investigator
- Doxorubicin-induced Cardiotoxicity: the Role of Topoisomerase 2b NIH Principal Investigator
- De-SUMOylation and the Hypoxic Response NIH Principal Investigator
- STUDIES OF THE SENTRIN FAMILY OF UBIQUITIN-LIKE PROTEINS NIH Principal Investigator
- PATHOBIOLOGY OF PAROXYSMAL NOCTURNAL HEMOGLOBINURIA NIH Principal Investigator
Collaboration Network
Top Collaborators
- Impaired Kv7 channel activity in the central amygdala contributes to elevated sympathetic outflow in hypertension
- Dipeptidylpeptidase 4 promotes survival and stemness of acute myeloid leukemia stem cells
- Signaling pathways involved in NMDA ‐induced suppression of M‐channels in corticotropin‐releasing hormone neurons in central amygdala
- Prevention of Heart Failure Induced by Doxorubicin with Early Administration of Dexrazoxane (PHOENIX Study): dose response and time course of dexrazoxane-induced degradation of topoisomerase 2b
- Microglia‐Mediated Synaptic Dysfunction Contributes to Chemotherapy‐Related Cognitive Impairment
Showing 5 of 8 shared publications
- Corticotropin-releasing hormone neurons in the central nucleus of amygdala are required for chronic stress-induced hypertension
- Dipeptidylpeptidase 4 promotes survival and stemness of acute myeloid leukemia stem cells
- Signaling pathways involved in NMDA ‐induced suppression of M‐channels in corticotropin‐releasing hormone neurons in central amygdala
- Microglia‐Mediated Synaptic Dysfunction Contributes to Chemotherapy‐Related Cognitive Impairment
- Dependence of Acute Myeloid Leukemia Development on Membrane Protein Dipeptidyl Peptidase 4
- Impaired Kv7 channel activity in the central amygdala contributes to elevated sympathetic outflow in hypertension
- Corticotropin-releasing hormone neurons in the central nucleus of amygdala are required for chronic stress-induced hypertension
- Signaling pathways involved in NMDA ‐induced suppression of M‐channels in corticotropin‐releasing hormone neurons in central amygdala
- Microglia‐Mediated Synaptic Dysfunction Contributes to Chemotherapy‐Related Cognitive Impairment
- Impaired Kv7 channel activity in the central amygdala contributes to elevated sympathetic outflow in hypertension
- Corticotropin-releasing hormone neurons in the central nucleus of amygdala are required for chronic stress-induced hypertension
- Signaling pathways involved in NMDA ‐induced suppression of M‐channels in corticotropin‐releasing hormone neurons in central amygdala
- Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation in mice
- L’excès de SUMOylation altère l’homéostasie postnatale du cortex surrénalien et conduit à un déficit isolé en glucocorticoïde
- Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation
- Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation in mice
- L’excès de SUMOylation altère l’homéostasie postnatale du cortex surrénalien et conduit à un déficit isolé en glucocorticoïde
- Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation
- Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation in mice
- L’excès de SUMOylation altère l’homéostasie postnatale du cortex surrénalien et conduit à un déficit isolé en glucocorticoïde
- Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation
- Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation in mice
- L’excès de SUMOylation altère l’homéostasie postnatale du cortex surrénalien et conduit à un déficit isolé en glucocorticoïde
- Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation
- Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation in mice
- L’excès de SUMOylation altère l’homéostasie postnatale du cortex surrénalien et conduit à un déficit isolé en glucocorticoïde
- Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation
- Corticotropin-releasing hormone neurons in the central nucleus of amygdala are required for chronic stress-induced hypertension
- Regulation of TLR4 signaling through the TRAF6/sNASP axis by reversible phosphorylation mediated by CK2 and PP4
- PP4 modulates macrophage-neutrophil crosstalk to restrict CCL5 -driven NETosis in sepsis
- Impaired Kv7 channel activity in the central amygdala contributes to elevated sympathetic outflow in hypertension
- Corticotropin-releasing hormone neurons in the central nucleus of amygdala are required for chronic stress-induced hypertension
- Impaired Kv7 channel activity in the central amygdala contributes to elevated sympathetic outflow in hypertension
- Corticotropin-releasing hormone neurons in the central nucleus of amygdala are required for chronic stress-induced hypertension
- Impaired Kv7 channel activity in the central amygdala contributes to elevated sympathetic outflow in hypertension
- Corticotropin-releasing hormone neurons in the central nucleus of amygdala are required for chronic stress-induced hypertension
- Impaired Kv7 channel activity in the central amygdala contributes to elevated sympathetic outflow in hypertension
- Corticotropin-releasing hormone neurons in the central nucleus of amygdala are required for chronic stress-induced hypertension
- SENP2-PLCβ4 signaling regulates neurogenesis through the maintenance of calcium homeostasis
- The SUMO-specific protease SENP2 plays an essential role in the regulation of Kv7.2 and Kv7.3 potassium channels
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