Results 91 to 100 of about 801,889 (178)

FGF10 promotes regional foetal cardiomyocyte proliferation and adult cardiomyocyte cell-cycle re-entry

, 2020
© The Author 2014. Aims Cardiomyocyte proliferation gradually declines during embryogenesis resulting in severely limited regenerative capacities in the adult heart.
Bennett M., Mohun T., Bellusci S., Chao C., Sturny R., Rochais F., Mesbah K., Kelly R.   +7 more
core  

Cardiomyocyte proliferation and heart regeneration in adult Xenopus tropicalis evidenced by a transgenic reporter line. [PDF]

NPJ Regen Med
Cardiomyocyte proliferation in adult Xenopus tropicalis during heart regeneration has remained largely contentious due to the absence of genetic evidence.
Lin XL, Lin JH, Cao Y, Zhang H, He SY, Wu HY, Ye ZB, Zheng L, Qi XF.   +8 more
europepmc   +2 more sources

Regulation of cardiomyocyte proliferation by Foxp1 [PDF]

Cell Cycle, 2010
Yuzhen, Wang, Edward, Morrisey
openaire   +2 more sources

Cardiomyocyte Foxp1‐Specific Deletion Promotes Post‐injury Heart Regeneration via Targeting Usp20‐HIF1ɑ‐Hand1 Signaling Pathway

Advanced Science
The adult mammalian heart has limited regenerative capacity to replace lost tissue after a major injury. Forkhead box P1 (Foxp1) regulates embryonic cardiomyocyte proliferation and heart development.
Yanfang Wang, Xiaoyu Wang, Ji Fang, Xiaoli Chen, Teng Xu, Tao Zhuang, Sheng Peng, Wenzhen Bao, Wenrun Wu, Yushi Lu, Haikun Wang, Brian Tomlinson, Paul Chan, Shougang Zhuang, Qi Zhang, Lin Zhang, Zhongmin Liu, Jingjiang Pi, Yuzhen Zhang, Jie Liu   +19 more
doaj   +1 more source

Identification of circular RNAs regulating cardiomyocyte proliferation in neonatal pig hearts. [PDF]

JCI Insight
Circular RNAs Regulating Cardiomyocyte Proliferation in Neonatal Pig HeartsTHIS DATASET IS ARCHIVED AT DANS/EASY, BUT NOT ACCESSIBLE HERE.
Tang L, Nyarige V, Li P, Wang J, Zhu W.
europepmc   +2 more sources

Mitochondrial-to-nuclear communications through multiple routes regulate cardiomyocyte proliferation

Cell Regeneration
The regenerative capacity of the adult mammalian heart remains a formidable challenge in biological research. Despite extensive investigations into the loss of regenerative potential during evolution and development, unlocking the mechanisms governing ...
Xinhang Li, Yalin Zhu, Pilar Ruiz-Lozano, Ke Wei   +3 more
doaj   +1 more source

Human Ventricular Unloading Induces Cardiomyocyte Proliferation

Journal of the American College of Cardiology, 2015
The adult mammalian heart is incapable of meaningful regeneration after substantial cardiomyocyte loss, primarily due to the inability of adult cardiomyocytes to divide. Our group recently showed that mitochondria-mediated oxidative DNA damage is an important regulator of postnatal cardiomyocyte cell cycle arrest.
Canseco, Diana C., Kimura, Wataru, Garg, Sonia, Mukherjee, Shibani, Bhattacharya, Souparno, Abdisalaam, Salim, Das, Sandeep, Asaithamby, Aroumougame, Mammen, Pradeep P.A., Sadek, Hesham A.   +9 more
openaire   +2 more sources

TEAD1 is regulator of cardiomyocyte proliferation and differentiation

, 2019
Heart development is a tightly regulated process directed to control cardiomyocyte proliferation and differentiation. After birth, cardiomyocytes steadily lose the ability to proliferate and the heart growth is maintained by physiological hypertrophy and
Renkawitz-Pohl, Renate (Prof. Dr. ), Zarjitskaya-Thierling, Polina   +1 more
core   +1 more source

ErbB2 is required for cardiomyocyte proliferation in murine neonatal hearts [PDF]

, 2016
It has been long recognized that the mammalian heart loses its proliferative capacity soon after birth, yet, the molecular basis of this loss of cardiac proliferation postnatally is largely unknown. In this study, we found that cardiac ErbB2, a member of
Qian, Li, Liu, Jiandong, Yin, Chaoying, Zhang, Yingao, Ma, Hong   +4 more
core   +1 more source

Cardiomyocyte Proliferation: A Platform for Mammalian Cardiac Repair [PDF]

Cell Cycle, 2005
Permanent loss of heart muscle cells, cardiomyocytes, is a major mechanism resulting in ventricular dysfunction and heart failure. Potential solutions to this problem could be either to stimulate the heart to generate new cells by inducing existing cardiomyocytes to divide or to activate or deliver stem cells/ progenitor cells to multiply and ...
openaire   +2 more sources