Fig. 1.

Senescence genesis, organelle specific molecular pathways consequences. Environmental stresses including ionizing radiation, cytotoxic agents and stress cause cells to express the senescent phenotype. Senescent cells are characterized by (1) increased lysosomal activity and decreased autophagy (2) expression of histone γ-H2AX (a marker of DNA strand breaks and telomere shortening), increased p16 and p21 (indicative of cell cycle arrest) and DDR (DNA damage response, an evolutionarily conserved signaling cascade, and (3) increased production of reactive oxygen species. These collectively promote a proinflammatory senescence associated secretory phenotype (SASP). The consequence of these processes increases chronic inflammation and fibrosis, promotes tissue remodeling and alters both innate and adaptive immunity