Programmed cell death (PCD) pathways, including apoptosis and regulated necrosis, are required for normal cell turnover and tissue homeostasis. Mis-regulation of PCD is increasingly implicated in aging and aging-related disease. During aging the cell turnover rate declines for several highly-mitotic tissues. Aging-associated disruptions in systemic and inter-cell signaling combined with cell-autonomous damage and mitochondrial malfunction result in increased PCD in some cell types, and decreased PCD in other cell types. Increased PCD during aging is implicated in immune system decline, skeletal muscle wasting (sarcopenia), loss of cells in the heart, and neurodegenerative disease. In contrast, cancer cells and senescent cells are resistant to PCD, enabling them to increase in abundance during aging. PCD pathways limit life span in fungi, but whether PCD pathways normally limit adult metazoan life span is not yet clear. PCD is regulated by a balance of negative and positive factors, including the mitochondria, which are particularly subject to aging-associated malfunction.

中文翻译：

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程序性衰老中的细胞死亡。

正常细胞更新和组织动态平衡需要程序性细胞死亡（PCD）途径，包括凋亡和调节性坏死。PCD的调控异常与衰老及与衰老相关的疾病越来越多。在衰老期间，几种高度有丝分裂的组织的细胞更新率下降。与衰老相关的全身性和细胞间信号传导破坏与细胞自主性损伤和线粒体功能障碍相结合，导致某些细胞类型的PCD升高，而其他细胞类型的PCD降低。衰老过程中PCD升高与免疫系统下降，骨骼肌消瘦（肌肉减少症），心脏细胞丢失和神经退行性疾病有关。相反，癌细胞和衰老细胞对PCD具有抗性，从而使它们能够在衰老过程中增加丰度。PCD途径限制了真菌的寿命，但是，PCD途径是否通常会限制成年后生动物的寿命尚不清楚。PCD受负和正因素（包括线粒体）平衡的调节，这些因素尤其容易引起与衰老相关的故障。