Hui‐Ming Chang
Professor
Faculty Researcher
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Hui-Ming Chang's research program focuses on understanding the molecular and cellular mechanisms underlying disease, with a particular emphasis on cardiovascular conditions and cancer. Chang has investigated the role of specific ion channels, such as Kv7 channels, in the central amygdala and their contribution to elevated sympathetic outflow in hypertension. This work has explored the involvement of corticotropin-releasing hormone neurons in stress-induced hypertension and the signaling pathways, including NMDA receptor activity, that modulate neuronal function.
In parallel, Chang's laboratory studies acute myeloid leukemia stem cells, identifying dipeptidylpeptidase 4 as a promoter of their survival and stemness. Further research extends to chemotherapy-induced cognitive impairment, examining the role of microglia-mediated synaptic dysfunction. A significant portion of Chang's funded work, supported by a $489,570 NIH/NHLBI grant, investigates the prevention of doxorubicin-induced heart failure and the dose-response and time course of dexrazoxane's effects on topoisomerase 2b degradation. Chang holds a high-impact researcher designation, evidenced by an h-index of 23 and over 2,800 citations across 66 publications, and collaborates with researchers Edward T.H. Yeh and J.C. Hsu at the University of Arkansas for Medical Sciences.
Metrics
- h-index: 23
- Publications: 66
- Citations: 2,835
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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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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Corticotropin-releasing hormone neurons in the central nucleus of amygdala are required for chronic stress-induced hypertension (2023)
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Dipeptidylpeptidase 4 promotes survival and stemness of acute myeloid leukemia stem cells (2023)
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Signaling pathways involved in <scp>NMDA</scp>‐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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Abstract 9710: Prevention of Doxorubicin-Induced Cardiotoxicity Through Targeted Degradation of Topoisomerase 2b (2021)
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Regulation of TLR4 signaling through the TRAF6/sNASP axis by reversible phosphorylation mediated by CK2 and PP4 (2021)
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Impaired Kv7 channel activity in the central amygdala contributes to elevated sympathetic outflow in hypertension (2021)
Federal Grants 1 $489,570 total
Prevention of Heart Failure induced by Doxorubicin with Early Administration of Dexrazoxane
Grants & Funding
As listed on this researcher's institutional profile. Federal awards with verified records are shown above.
- PATHOBIOLOGY OF PAROXYSMAL NOCTURNAL HEMOGLOBINURIA NIH
- STUDIES OF THE SENTRIN FAMILY OF UBIQUITIN-LIKE PROTEINS NIH
- PATHOBIOCHEMISTRY OF ACUTE PROMYELOCYTIC LEUKEMIA NIH
Collaboration Network
Top Collaborators
- 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
- Regulation of TLR4 signaling through the TRAF6/sNASP axis by reversible phosphorylation mediated by CK2 and PP4
- Dipeptidylpeptidase 4 promotes survival and stemness of acute myeloid leukemia stem cells
- Signaling pathways involved in <scp>NMDA</scp>‐induced suppression of M‐channels in corticotropin‐releasing hormone neurons in central amygdala
Showing 5 of 10 shared publications
- 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 <scp>NMDA</scp>‐induced suppression of M‐channels in corticotropin‐releasing hormone neurons in central amygdala
- Microglia‐Mediated Synaptic Dysfunction Contributes to Chemotherapy‐Related Cognitive Impairment
- 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
- 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 <scp>NMDA</scp>‐induced suppression of M‐channels in corticotropin‐releasing hormone neurons in central amygdala
- 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
- Dipeptidylpeptidase 4 promotes survival and stemness of acute myeloid leukemia stem cells
- Dependence of Acute Myeloid Leukemia Development on Membrane Protein Dipeptidyl Peptidase 4
- Dipeptidylpeptidase 4 promotes survival and stemness of acute myeloid leukemia stem cells
- Dependence of Acute Myeloid Leukemia Development on Membrane Protein Dipeptidyl Peptidase 4
- Dipeptidylpeptidase 4 promotes survival and stemness of acute myeloid leukemia stem cells
- Dependence of Acute Myeloid Leukemia Development on Membrane Protein Dipeptidyl Peptidase 4
- Dipeptidylpeptidase 4 promotes survival and stemness of acute myeloid leukemia stem cells
- Dependence of Acute Myeloid Leukemia Development on Membrane Protein Dipeptidyl Peptidase 4
- Dipeptidylpeptidase 4 promotes survival and stemness of acute myeloid leukemia stem cells
- Dependence of Acute Myeloid Leukemia Development on Membrane Protein Dipeptidyl Peptidase 4
- Dipeptidylpeptidase 4 promotes survival and stemness of acute myeloid leukemia stem cells
- Dependence of Acute Myeloid Leukemia Development on Membrane Protein Dipeptidyl Peptidase 4
- Signaling pathways involved in <scp>NMDA</scp>‐induced suppression of M‐channels in corticotropin‐releasing hormone neurons in central amygdala
- Microglia‐Mediated Synaptic Dysfunction Contributes to Chemotherapy‐Related Cognitive Impairment
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