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Dr. Sean Wu is an Associate Professor of Medicine at the Stanford School of Medicine. The Wu lab seeks to identify mechanisms responsible for human congenital heart disease, and uses mouse models and stem cells to study cardiovascular developmental biology, and to engineer cardiac tissue.
hESC-Derived Dopamine Progenitors for Parkinson’s Treatment– Researchers have generated midbrain dopamine neurons from hESCs, and manufactured large-scale cryopreserved dopamine progenitors for clinical use in the treatment of Parkinson’s disease.
Reactivating Neural Crest Pluripotency – A new study suggests that cranial neural crest cells expand their developmental potential through a transient reacquisition of molecular signatures of pluripotency.
Engaging Eosinophils against Liver Injury – Scientists have discovered a mechanism of eosinophil-mediated liver protection that could serve as a therapeutic target to improve outcomes of patients undergoing liver transplantation.
Disrupting the Identity of Heart Muscle Cells – Mutations in the LMNA gene severely disrupt chromatin organization in cardiomyocytes, but not hepatocytes or adipocytes, leading to abnormal activation of non-heart muscle genes.
Photo Reference: Courtesy of Dr. Sean Wu
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By The Stem Cell Podcast4.7
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Dr. Sean Wu is an Associate Professor of Medicine at the Stanford School of Medicine. The Wu lab seeks to identify mechanisms responsible for human congenital heart disease, and uses mouse models and stem cells to study cardiovascular developmental biology, and to engineer cardiac tissue.
hESC-Derived Dopamine Progenitors for Parkinson’s Treatment– Researchers have generated midbrain dopamine neurons from hESCs, and manufactured large-scale cryopreserved dopamine progenitors for clinical use in the treatment of Parkinson’s disease.
Reactivating Neural Crest Pluripotency – A new study suggests that cranial neural crest cells expand their developmental potential through a transient reacquisition of molecular signatures of pluripotency.
Engaging Eosinophils against Liver Injury – Scientists have discovered a mechanism of eosinophil-mediated liver protection that could serve as a therapeutic target to improve outcomes of patients undergoing liver transplantation.
Disrupting the Identity of Heart Muscle Cells – Mutations in the LMNA gene severely disrupt chromatin organization in cardiomyocytes, but not hepatocytes or adipocytes, leading to abnormal activation of non-heart muscle genes.
Photo Reference: Courtesy of Dr. Sean Wu
Never miss updates about new episodes.

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