线粒体-内质网 (ER) 接触位点 (MERCS) 作为调节基本细胞功能的瞬时信号平台。 MERCS 富含将线粒体和 ER 连接在一起并调节其活性的特定蛋白质和脂质。 MERCS 失调与多种人类疾病有关，包括阿尔茨海默病 (AD)、帕金森病 (PD) 和癌症。 BCL-2 家族蛋白除了在线粒体凋亡中发挥作用外，还可以定位于 MERCS 并控制钙信号传导和自噬等基本细胞功能。此外，最近发现 BCL-2 介导的细胞凋亡机制可触发 cGAS-STING 通路激活和促炎症反应，这是这些需要线粒体-ER 相互作用的疾病的公认标志。本综述强调了 MERCS 在调节基本细胞功能中的关键作用，重点关注它们与 BCL-2 家族蛋白的串扰，并讨论了它们的失调如何与疾病相关。版权所有 © 2024 作者。由爱思唯尔有限公司出版。保留所有权利。

Mitochondria-endoplasmic reticulum (ER) contact sites (MERCS) function as transient signaling platforms that regulate essential cellular functions. MERCS are enriched in specific proteins and lipids that connect mitochondria and the ER together and modulate their activities. Dysregulation of MERCS is associated with several human pathologies including Alzheimer's disease (AD), Parkinson's disease (PD), and cancer. BCL-2 family proteins can locate at MERCS and control essential cellular functions such as calcium signaling and autophagy in addition to their role in mitochondrial apoptosis. Moreover, the BCL-2-mediated apoptotic machinery was recently found to trigger cGAS-STING pathway activation and a proinflammatory response, a recognized hallmark of these diseases that requires mitochondria-ER interplay. This review underscores the pivotal role of MERCS in regulating essential cellular functions, focusing on their crosstalk with BCL-2 family proteins, and discusses how their dysregulation is linked to disease.Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.