Laboratory of Eunhee Kim, Ph.D.


Research in the Eunhee Kim laboratory is focused on evaluating molecular and genetic mechanisms, biomarkers, and the inflammatory response involved in stroke and brain arteriovenous malformation (bAVM). The ultimate research goal is to translate the findings into novel therapeutic strategies for the patients.

Stroke is one of the major causes of disability and death worldwide, however there are limited treatment options available for the stroke patients. Several risk factors such as hypertension, dyslipidemia, and diabetes have been involved in the higher stroke incidence and poorer outcomes, but the underlying mechanism(s) of the negative impact is not clear. By incorporating the risk factors in animal models of stroke, Dr. Kim is particularly interested in investigating how post-stroke stress response is regulated in the comorbid conditions, and how it affects stroke-induced immune response and stroke outcomes including acute injury and long-term recovery.

Another line of research is focused on understanding the pathophysiology of brain arteriovenous malformation (bAVM). The bAVM is a critical risk factor for hemorrhagic stroke in young patients however, the etiology and pathology of bAVM are largely unknown. Dr. Kim is currently investigating the role of several molecular factors related to endothelial dysfunction, angiogenesis, and inflammation in bAVM pathophysiology. By modulating the factors in vivo and in vitro, the ongoing bAVM research includes generating a clinically-relevant bAVM animal models and defining the underlying mechanisms in bAVM formation and pathology, and investigating the subsequent impact of bAVM in cerebral hemorrhage.

Dr. Eunhee Kim is an assistant Professor in Vivian L. Smith Department of Neurosurgery at UTHealth Houston. Dr. Kim received her Ph.D at Kyung Hee University in Seoul, Korea. During her Ph.D, she focused on the regulation of growth hormone axis in endocrine disorders such as acromegaly and diabetes. With the background in neuroendocrinology, she joined Dr. Cho lab at Burke Medical Research Institute for a postdoctoral training and was promoted as an instructor in Feil Family Brain and Mind Research institute at Weill Cornell Medicine in 2013. During the training and early career period, Dr. Kim acquired an extensive experience in cerebrovascular pathophysiology with a specific training in in vivo and in vitro studies on ischemic stroke. She defined the role of an inflammatory mediator, CD36 in acute stroke outcomes in hyperlipidemic and diabetic conditions and the underlying mechanisms governing the stroke with the comorbidities. She was also involved in studying the importance of synaptic plasticity for long-term functional recovery after stroke and the effect of genetics using animal model of human BDNF polymorphism. These works have been published in several journals including Annals of Neurology, Journal of Neuroscience, and Journal of Cerebral Blood Flow and Metabolism.


  • Effect of stress response on acute stroke injury and long term recovery in diabetic condition
  • Role of brain endothelial KRAS mutation in bAVM formation and pathology
  • Role of neuroinflammatory response in endothelial dysfunction and bAVM pathology


Eunhee Kim, PhD
Eunsu Park, PhD, Postdoctoral Research Fellow



Office Phone: 713-500-6837


  1. Kim E, Yang J, Park KW, Cho S (2017) Inhibition of VEGF Signaling Reduces Diabetes-Exacerbated Brain Swelling, but Not Infarct Size, in Large Cerebral Infarction in Mice. Transl Stroke Res, 2018 Oct;9(5):540-548. doi: 10.1007/s12975-017-0601-z. Epub 2017 Dec 30. PMCID: PMC6057840
  2. Kim E, Cho S (2016) Microglia and Monocyte-Derived Macrophages in Stroke. Neurotherapeutics, Oct;13(4):702-718 doi: 1007/s13311-016-0463-1 PMCID: PMC5081116
  3. Kim E, Woo MS, Qin L, Ma T, Beltran CD, Bao Y, Bailey JA, Corbett D, Ratan RR, Lahiri DK, Cho S. (2015) Daidzein Augments Cholesterol Homeostasis via ApoE to Promote Functional Recovery in Chronic Stroke, J Neurosci. Nov 11;35(45):15113-26. doi: 10.1523/JNEUROSCI.2890-15.2015. PMCID: PMC4642242
  4. Kim E, Tolhurst AT, Szeto HH, Cho S. (2014) Targeting CD36-mediated inflammation reduces acute brain injury in transient, but not permanent, ischemic stroke. CNS Neurosci Ther. Apr;21(4):385-91. doi: 10.1111/cns.12326. PMCID: PMC4362808
  5. Kim E, Yang J, Beltran CD, Cho S. (2014) Spleen-derived monocytes/macrophages are not necessary for acute ischemic brain injury. J Cereb Blood flow Metab. Aug;34(8):1411-9. doi: 10.1038/jcbfm.2014.101. Epub 2014 May 28. PMCID: PMC4126087
  6. Kim E, Tolhurst AT, Cho S. (2014) Deregulation of inflammatory response in the diabetic condition is associated with increased ischemic brain injury, J Neuroinflammation, May 1;11(1):83. doi: 10.1186/1742-2094-11-83. PMCID: PMC4017808.
  7. Bao Y, Qin L, Kim E, Bhosle S, Guo H, Febbraio M, Haskew-Layton RE, Ratan R, Cho S. (2012) CD36 is involved in astrocyte activation and astroglial scar J Cereb Blood Flow Metab. 2012 Aug;32(8):1567-77. doi: 10.1038/jcbfm.2012.52. Epub 2012 Apr 18. PMCID: PMC3421096
  8. Kim E, Febbraio E, Bao Y, Tolhurst AT, Epstein JM, Cho S. (2012) CD36 in the periphery and brain synergizes in stroke injury in hyperlipidemia. Ann Neurol, Jun; 71(6):753-64. PMCID: PMC3383818
  9. Basso M, Berlin J, Xia L, Sleiman S, Ko B, Haskew-Layton RE, Kim E, Antonyak M, Cerione R, Iismaa S, Willis D, Cho S, Ratan R. (2012) Transglutaminase inhibition protects against oxidative stress-induced neuronal death downstream of pathological ERK activation. J Neurosci. May 9;32(19):6561-9. PMCID: PMC3444816
  10. Qin L, Kim E, Ratan R, Lee FS, Cho S (2011) Genetic variant of BDNF (Val66Met) polymorphism attenuates stroke-induced angiogenic responses by enhancing anti-angiogenic mediator CD36 expression. J Neurosci. Jan 12;31(2):775-83. PMCID: PMC3308129
  11. Bao Y, Kim E, Bhosle S, Mehta H, Cho S (2010) A role for spleen monocytes in post-ischemic brain inflammation and injury. J Neuroinflammation Dec 15;7:92. PMCID: PMC3016273

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