Molecular Metabolism, Lund University Diabetes Centre, Malmö -21428, Sweden.
School of Biotechnology, Jawaharlal Nehru University, -110067, New Delhi, India.
J Diabetes Res. 2020 Oct 8;2020:7814628. doi: 10.1155/2020/7814628. eCollection 2020.
The role of mitochondria in apoptosis is well known; however, the mechanisms linking mitochondria to the proapoptotic effects of proinflammatory cytokines, hyperglycemia, and glucolipotoxicity are not completely understood. Complex Ca signaling has emerged as a critical contributor to these proapoptotic effects and has gained significant attention in regulating the signaling processes of mitochondria. In pancreatic -cells, Ca plays an active role in -cell function and survival. Prohibitin (PHB), a mitochondrial chaperone, is actively involved in maintaining the architecture of mitochondria. However, its possible interaction with Ca-activated signaling pathways has not been explored. The present review aims to examine potential crosstalk between Ca signaling and PHB function in pancreatic -cells. Moreover, this review will focus on the effects of cytokines and glucolipotoxicity on Ca signaling and its possible interaction with PHB. Improved understanding of this important mitochondrial protein may aid in the design of more targeted drugs to identify specific pathways involved with stress-induced dysfunction in the -cell.
线粒体在细胞凋亡中的作用是众所周知的；然而，将线粒体与促炎细胞因子、高血糖和糖脂毒性的促凋亡作用联系起来的机制尚不完全清楚。复杂的钙信号已成为这些促凋亡作用的关键贡献者，并在调节线粒体的信号转导过程中引起了广泛关注。在胰岛细胞中，Ca 离子在胰岛细胞功能和存活中发挥着积极的作用。抑素（PHB），一种线粒体伴侣蛋白，积极参与维持线粒体的结构。然而，其与 Ca 激活的信号通路的可能相互作用尚未被探索。本综述旨在探讨胰岛细胞中 Ca 信号与 PHB 功能之间的潜在串扰。此外，本综述将重点关注细胞因子和糖脂毒性对 Ca 信号的影响及其与 PHB 的可能相互作用。对这种重要的线粒体蛋白的深入了解可能有助于设计更有针对性的药物，以确定应激诱导的 - 细胞功能障碍涉及的特定途径。
