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Although stroke is a primary cause of disability and death in the U.S., few options exist for treating patients who have had a stroke. The paucity of treatment options has prompted the field to focus on identification and validation of potential targets for developing treatment strategies. Focused on preclinical stroke studies on in vivo pathology, my lab closely examines stroke pathology and addresses a gap between preclinical and clinical settings for translational medicine.
Two main lines of research have been established in my laboratory; acute pathology/neuroprotection and long-term stroke recovery. For the former, we has been examined several well known risk factors associated with higher incidence of vascular diseases including hypercholesterolemia, diabetes, and obesity, and systematically examined their effect on stroke outcome in experimental animal models of stroke. In addition, close examination of stroke pathology revealed involvement of multiple-pro-death processes including inflammation, apoptosis, oxidative stress, and vascular dysfunction. Thus, targeting a specific pathway may not overcome the heterogeneous nature of stroke pathology. This led to the concept of a multi-modal approach: targeting a molecule that is involved in multiple pathogenesis, thereby simultaneously mitigating pro-death pathways. To this end, we proposed that CD36, a class B scavenger receptor, is a potential target molecule for a multi-modal approach. We have been particularly focuses on in vivo phenomena and the underlying events by which peripheral inflammatory status influences the acute outcome of stroke-induced injury through a novel CD36 mechanism.
Two main lines of research have been established in my laboratory; acute pathology/neuroprotection and long-term stroke recovery. For the former, we has been examined several well known risk factors associated with higher incidence of vascular diseases including hypercholesterolemia, diabetes, and obesity, and systematically examined their effect on stroke outcome in experimental animal models of stroke. In addition, close examination of stroke pathology revealed involvement of multiple-pro-death processes including inflammation, apoptosis, oxidative stress, and vascular dysfunction. Thus, targeting a specific pathway may not overcome the heterogeneous nature of stroke pathology. This led to the concept of a multi-modal approach: targeting a molecule that is involved in multiple pathogenesis, thereby simultaneously mitigating pro-death pathways. To this end, we proposed that CD36, a class B scavenger receptor, is a potential target molecule for a multi-modal approach. We have been particularly focuses on in vivo phenomena and the underlying events by which peripheral inflammatory status influences the acute outcome of stroke-induced injury through a novel CD36 mechanism.
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Il-doo Kim,Hyunwoo Ju, Joseph Minkler, Roselyn Jiang,Abhilasha Singh, Roopa Sharma,Maria Febbraio,Sunghee Cho
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISMno. 6 (2023): 843-855
European journal of neurologyno. 2 (2023): e16111-e16111
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISMpp.271678X231215101-271678X231215101, (2023)
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NEURONno. 18 (2023): 2831-2846
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SSRN Electronic Journal (2022)
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