Role of PTEN-less in cardiac injury, hypertrophy and regeneration
Open Access
- 2 August 2021
- journal article
- review article
- Published by Springer Science and Business Media LLC in Cell Regeneration
- Vol. 10 (1), 1-11
- https://doi.org/10.1186/s13619-021-00087-3
Abstract
Cardiovascular diseases are the leading cause of death worldwide. Cardiomyocytes are capable of coordinated contractions, which are mainly responsible for pumping blood. When cardiac stress occurs, cardiomyocytes undergo transition from physiological homeostasis to hypertrophic growth, proliferation, or apoptosis. During these processes, many cellular factors and signaling pathways participate. PTEN is a ubiquitous dual-specificity phosphatase and functions by dephosphorylating target proteins or lipids, such as PIP3, a second messenger in the PI3K/AKT signaling pathway. Downregulation of PTEN expression or inhibiting its biologic activity improves heart function, promotes cardiomyocytes proliferation, reduces cardiac fibrosis as well as dilation, and inhibits apoptosis following ischemic stress such as myocardial infarction. Inactivation of PTEN exhibits a potentially beneficial therapeutic effects against cardiac diseases. In this review, we summarize various strategies for PTEN inactivation and highlight the roles of PTEN-less in regulating cardiomyocytes during cardiac development and stress responses.Keywords
Funding Information
- National Natural Science Foundation of China (81670257, 81970227, 82000244)
- Natural Science Foundation of Zhejiang Province (LZ20H020001)
- Postdoctoral Research Foundation of China (2020M671751, 2021T140596)
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