Asset Details
Do you wish to reserve the book?
LRP6 downregulation promotes cardiomyocyte proliferation and heart regeneration
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
LRP6 downregulation promotes cardiomyocyte proliferation and heart regeneration
Do you wish to request the book?
LRP6 downregulation promotes cardiomyocyte proliferation and heart regeneration
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
LRP6 downregulation promotes cardiomyocyte proliferation and heart regeneration
2021
Overview
The adult mammalian heart is thought to be a terminally differentiated organ given the postmitotic nature of cardiomyocytes. Consequently, the potential for cardiac repair through cardiomyocyte proliferation is extremely limited. Low-density lipoprotein receptor-related protein 6 (LRP6) is a Wnt co-receptor that is required for embryonic heart development. In this study we investigated the role of LRP6 in heart repair through regulation of cardiomyocyte proliferation.
Lrp6
deficiency increased cardiomyocyte cell cycle activity in neonatal, juvenile and adult mice. Cardiomyocyte-specific deletion of
Lrp6
in the mouse heart induced a robust regenerative response after myocardial infarction (MI), led to reduced MI area and improvement in left ventricular systolic function. In vivo genetic lineage tracing revealed that the newly formed cardiomyocytes in
Lrp6
-deficient mouse hearts after MI were mainly derived from resident cardiomyocytes. Furthermore, we found that the pro-proliferative effect of
Lrp6
deficiency was mediated by the ING5/P21 signaling pathway. Gene therapy using the adeno-associated virus (AAV)9 miRNAi
-Lrp6
construct promoted the repair of heart injury in mice.
Lrp6
deficiency also induced the proliferation of human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs). Our study identifies LRP6 as a critical regulator of cardiomyocyte proliferation, which may lead to the development of a novel molecular strategy to promote myocardial regeneration and repair.
Publisher
Springer Singapore,Nature Publishing Group
Subject
/ 13/109
/ 13/44
/ 13/51
/ 13/89
/ 14/19
/ 14/63
/ 38/77
/ 38/90
/ 38/91
/ 64/60
/ 82/80
/ Animals
/ Biomedical and Life Sciences
/ Heart
/ Humans
/ Induced Pluripotent Stem Cells - cytology
/ Induced Pluripotent Stem Cells - metabolism
/ Low Density Lipoprotein Receptor-Related Protein-6 - antagonists & inhibitors
/ Low Density Lipoprotein Receptor-Related Protein-6 - genetics
/ Low Density Lipoprotein Receptor-Related Protein-6 - metabolism
/ Mice
/ Myocardial Infarction - pathology
/ Myocytes, Cardiac - cytology
/ Myocytes, Cardiac - metabolism
/ Neonates
/ Rats
