TY - JOUR
T1 - Harnessing the microRNA pathway for cardiac regeneration
AU - Giacca, Mauro
AU - Zacchigna, Serena
PY - 2015/12/1
Y1 - 2015/12/1
N2 - Mounting evidence over the last few years has indicated that the rate of cardiomyocyte proliferation, and thus the extent of cardiac renewal, is under the control of the microRNA network. Several microRNAs (e.g. miR-1) regulate expansion of the cardiomyocyte pool and its terminal differentiation during the embryonic life; some not only promote cardiomyocyte proliferation but also their de-differentiation towards an embryonic cell phenotype (e.g. the miR-302/367 cluster); a few others are involved in the repression of cardiomyocyte proliferation occurring suddenly after birth (e.g. the miR-15 family); others again are not physiologically involved in the regulation of cardiomyocyte turnover, but nevertheless are able to promote cardiomyocyte proliferation and cardiac regeneration when delivered exogenously (e.g. miR-199a-3p). With a few exceptions, the molecular mechanisms underlying the pro-proliferative effect of these microRNAs, most of which appear to act at the level of already differentiated cardiomyocytes, remain to be thoroughly elucidated. The possibility of harnessing the miRNA network to achieve cardiac regeneration paves the way to exciting therapeutic applications. This could be achieved by either administering miRNA mimics or inhibitors, or transducing the heart with viral vectors expressing miRNA-encoding genes.
AB - Mounting evidence over the last few years has indicated that the rate of cardiomyocyte proliferation, and thus the extent of cardiac renewal, is under the control of the microRNA network. Several microRNAs (e.g. miR-1) regulate expansion of the cardiomyocyte pool and its terminal differentiation during the embryonic life; some not only promote cardiomyocyte proliferation but also their de-differentiation towards an embryonic cell phenotype (e.g. the miR-302/367 cluster); a few others are involved in the repression of cardiomyocyte proliferation occurring suddenly after birth (e.g. the miR-15 family); others again are not physiologically involved in the regulation of cardiomyocyte turnover, but nevertheless are able to promote cardiomyocyte proliferation and cardiac regeneration when delivered exogenously (e.g. miR-199a-3p). With a few exceptions, the molecular mechanisms underlying the pro-proliferative effect of these microRNAs, most of which appear to act at the level of already differentiated cardiomyocytes, remain to be thoroughly elucidated. The possibility of harnessing the miRNA network to achieve cardiac regeneration paves the way to exciting therapeutic applications. This could be achieved by either administering miRNA mimics or inhibitors, or transducing the heart with viral vectors expressing miRNA-encoding genes.
KW - Biological therapeutics
KW - Cardiac regeneration
KW - Cell proliferation
KW - MicroRNA
KW - Myocardial infarction
UR - http://www.scopus.com/inward/record.url?scp=84952714823&partnerID=8YFLogxK
U2 - 10.1016/j.yjmcc.2015.09.017
DO - 10.1016/j.yjmcc.2015.09.017
M3 - Review article
C2 - 26431632
AN - SCOPUS:84952714823
SN - 0022-2828
VL - 89
SP - 68
EP - 74
JO - Journal of Molecular and Cellular Cardiology
JF - Journal of Molecular and Cellular Cardiology
ER -