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Senescent cell clearance refers to the **therapeutic removal or targeted destruction of senescent cells**, which are cells that have permanently exited the cell cycle in response to damage or stress and often secrete pro-inflammatory factors (the SASP). Accumulation of these cells is implicated in aging and multiple age-related diseases. Clearance can be achieved by pharmacological agents called senolytics, which induce apoptosis by disrupting survival pathways in senescent cells, or by stimulating the immune system (e.g., NK cells, macrophages, cytotoxic T cells) to recognize and remove these cells via ligands such as uPAR or through engineered cell therapies. While it is a major concept in gerontology and translational aging research, it is not a single molecular entity but rather a multifaceted therapeutic strategy acting through varied targets and pathways[1][2][3][4][5][6][8].
Inhibition of pro-survival/anti-apoptotic pathways in senescent cells (e.g., BCL-2, BCL-xL inhibition) - Modulation of senescence-associated secretory phenotype (SASP) (e.g., via JAK inhibitors, rapamycin, metformin) - Immune system activation or enhancement (e.g., chimeric antigen receptor-T cells against uPAR, vaccines against GPNMB) - Direct cytotoxicity to senescent cells
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