IMMP2L:a mitochondrial protease suppressing cellular senescence

• 来源期刊: 细胞研究（英文版）
• 年，卷（期）: 2018,（6）
• 页码范围: 607-608
• 页数: 2页
• 语种: 英文

摘要

Cellular senescence contributes to organismal aging and tumor suppression.A recent paper by Yuan et al.published in Cell Research now unveils that switching off a mitochondrial protease can simultaneously suppress phospholipid biosynthesis and lethal signaling for senescence induction. Organismal aging is coupled to the accumulation of senescent cells that,by definition,are permanently arrested in their cell cycle and often manifest the senescence-associated secretory phenotype (SASP),hence favoring chronic tissue inflammation.1 One prominent biomarker of cellular senescence is the enhanced expression of cyclin-dependent kinase (CDK) inhibitor 2A (CDKN2A,best known as p1 6).Genetic ablation of senescent cells by expressing inducible suicide genes under the control of the CDKN2A promoter can retard and reverse aging phenotypes in mice.2 That said,the phenomenon of cellular senescence also has important physiological functions,for instance in the suppression of oncogenesis (by irreversible arrest of the cell cycle in potentially malignant cells) and in wound healing (presumably because the SASP can favor local tissue repair).3