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Congenital and adult heart diseases are the leading causes of mortality worldwide. In Singapore, cardiovascular disease accounted for 30.4% of all deaths in 2011. Our laboratory studies the molecular mechanisms that regulate cardiovascular development, homeostasis and disease. Our goal is to understand how signaling pathways and transcriptional networks regulate cardiovascular cell lineages differentiation and their interaction during heart morphogenesis. Defects in these processes during embryonic development underlie congenital heart disease, and may contribute to the development of diseases in adulthood. Our work aims for better understanding of congenital human diseases of the heart by establishing mouse models for these disorders and delineating the molecular changes associated with them. Our long-term goal is to apply lessons learned from our developmental studies to better understand and treat cardiovascular diseases.
There are increasing evidences that molecules and signaling pathways required during embryonic development also play important role in cardiovascular tissue homeostasis in adults. For example, in a healthy adult heart, epicardial cells are thought to be generally quiescent. However, injury of the adult heart results in reactivation of a developmental gene program in the epicardium, which leads to increased epicardial cell proliferation and differentiation of epicardium-derived progenitor cells into various cardiac lineages. Given the limited capacity of the adult heart tissue for self-repair, significant effort has to be invested in regenerative strategies to replace damaged cardiac tissue and revascularise the heart. Our work will provide a better understanding of molecular mechanisms that regulate specification and differentiation of cardiovascular precursor cells into multiple cardiovascular lineages during repair/regeneration, which may provide means to reinitiate developmental programs for regenerative therapy.
There are increasing evidences that molecules and signaling pathways required during embryonic development also play important role in cardiovascular tissue homeostasis in adults. For example, in a healthy adult heart, epicardial cells are thought to be generally quiescent. However, injury of the adult heart results in reactivation of a developmental gene program in the epicardium, which leads to increased epicardial cell proliferation and differentiation of epicardium-derived progenitor cells into various cardiac lineages. Given the limited capacity of the adult heart tissue for self-repair, significant effort has to be invested in regenerative strategies to replace damaged cardiac tissue and revascularise the heart. Our work will provide a better understanding of molecular mechanisms that regulate specification and differentiation of cardiovascular precursor cells into multiple cardiovascular lineages during repair/regeneration, which may provide means to reinitiate developmental programs for regenerative therapy.
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Jia He,Adriana Blazeski, Uthayanan Nilanthi,Javier Menéndez, Samuel C Pirani,Daniel S Levic,Michel Bagnat,Manvendra K Singh, José G Raya,Guillermo García-Cardeña,Jesús Torres-Vázquez
bioRxiv : the preprint server for biology (2024)
BMC Genomicsno. 1 (2024): 1-8
bioRxiv (Cold Spring Harbor Laboratory) (2023)
Junjie Xu, Simon Erlendsson,Manvendra Singh,Matthew Regier, Iosune Ibiricu, Gregory S Day,Amanda L Piquet, Stacey L Clardy,Cedric Feschotte, John A G Briggs,Jason D Shepherd
bioRxiv : the preprint server for biology (2023)
Yiran Xie,Fangqi Zhao,Nancy Freitag,Sophia Borowski, Yiru Wang, Charlotte Harms,Poh-Choo Pang, Juliette Desforges, Tianyu Wen,Edzard Schwedhelm,Manvendra Singh,Ralf Dechend,
PNAS nexusno. 8 (2023): pgad247-pgad247
biorxiv(2023)
International journal of molecular sciencesno. 8 (2023): 7283-7283
bioRxiv (Cold Spring Harbor Laboratory) (2023)
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