Role of PTEN-less in cardiac injury, hypertrophy and regeneration.
Role of PTEN-less in cardiac injury, hypertrophy and regeneration.
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DOI：
10.1186/s13619-021-00087-3
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发表时间：
2021-08-02
期刊：
影响因子：
--
通讯作者：
Chen J
中科院分区：
文献类型：
--
作者：
Liang T;Gao F;Chen J
心血管疾病是全世界死亡的主要原因。心肌细胞能够协调收缩，主要负责泵血。当心脏应激发生时，心肌细胞经历从生理稳态到肥大生长、增殖或凋亡的转变。在这些过程中，许多细胞因子和信号通路参与。PTEN是一种普遍存在的双特异性磷酸酶，通过使靶蛋白或脂质（如PI 3 K/AKT信号通路中的第二信使PIP 3）去磷酸化而发挥作用。下调PTEN表达或抑制其生物学活性可改善心脏功能，促进心肌细胞增殖，减少心脏纤维化和扩张，并抑制缺血应激如心肌梗死后的细胞凋亡。失活的PTEN表现出潜在的有益的治疗作用，对心脏疾病。本文综述了PTEN失活的各种策略，并着重介绍了PTEN在心脏发育和应激反应中对心肌细胞的调控作用。
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.
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