Bcl-2 proteins are widely known as key controllers of mitochondrial outer membrane permeabilization, arguably the most important step of intrinsic apoptosis. Accumulating evidence indicate that most, if not all, members of the Bcl-2 protein family also mediate a number of apoptosis-unrelated functions. Intriguingly, many of these functions ultimately impinge on cell fate decisions via apoptosis-dependent or -independent mechanisms, delineating a complex network through which Bcl-2 family members regulate cell survival and death. Here, we critically discuss the mechanisms through which Bcl-2 proteins influence cell fate as they regulate autophagy, cellular senescence, inflammation, bioenergetic metabolism, Ca²⁺ fluxes, and redox homeostasis.

Bcl-2蛋白是众所周知的线粒体外膜通透性的关键控制因子，可以说是内在凋亡的最重要步骤。越来越多的证据表明，大多数（如果不是全部）Bcl-2蛋白家族成员还介导了许多与凋亡无关的功能。有趣的是，这些功能中的许多最终会通过凋亡依赖性或非依赖性机制影响细胞命运的决定，描绘出一个复杂的网络，Bcl-2家族成员通过该网络调节细胞存活和死亡。在这里，我们批判性地讨论Bcl-2蛋白质通过调节自噬，细胞衰老，炎症，生物能代谢，Ca ²⁺流量和氧化还原稳态来影响细胞命运的机制。