Sorriento Daniela, Gambardella Jessica, Fiordelisi Antonella, Iaccarino Guido, Illario Maddalena
Department of Advanced Biomedical Sciences, University of Naples Federico II, Naples, Italy.
Health Innovation Unit, Campania Region, Naples, Italy.
Front Pharmacol. 2019 Feb 12;10:64. doi: 10.3389/fphar.2019.00064. eCollection 2019.
Mitochondrial regulation of energy production, calcium homeostasis, and cell death are critical for cardiac function. Accordingly, the structural and functional abnormalities of these organelles (mitochondrial dysfunction) contribute to developing cardiovascular diseases and heart failure. Therefore the preservation of mitochondrial integrity is essential for cardiac cell survival. Mitochondrial function is regulated by several proteins, including GRK2 and β-arrestins which act in a GPCR independent manner to orchestrate intracellular signaling associated with key mitochondrial processes. It is now ascertained that GRK2 is able to recover mitochondrial function in response to insults. β-arrestins affect several intracellular signaling pathways within the cell which in turn are involved in the regulation of mitochondrial function, but a direct regulation of mitochondria needs further investigations. In this review, we discuss the recent acquisitions on the role of GRK2 and β-arrestins in the regulation of mitochondrial function.
线粒体对能量产生、钙稳态和细胞死亡的调节对心脏功能至关重要。因此，这些细胞器的结构和功能异常（线粒体功能障碍）会导致心血管疾病和心力衰竭的发生。所以，维持线粒体的完整性对心脏细胞存活至关重要。线粒体功能受多种蛋白质调节，包括GRK2和β-抑制蛋白，它们以GPCR非依赖的方式发挥作用，协调与关键线粒体过程相关的细胞内信号传导。现已确定，GRK2能够在受到损伤时恢复线粒体功能。β-抑制蛋白影响细胞内的多种细胞内信号通路，这些信号通路又参与线粒体功能的调节，但线粒体的直接调节还需要进一步研究。在这篇综述中，我们讨论了关于GRK2和β-抑制蛋白在调节线粒体功能中作用的最新研究成果。
