Target intelligence / Profile preview

Senescent cell clearance

Molecular classification
Other
01

Overview

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].

Other names
Senescent cell removalSenescent cell eliminationSenolytic therapy (when referring to pharmacological strategies)Clearance of senescent cells
02

Mechanism of action

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

03

Biological functions

Cell death (of senescent cells)Immune response (immune-mediated senescent cell clearance)Aging regulationTissue regeneration
04

Disease associations

CancerInflammationNeurodegenerative diseaseCardiovascular diseaseAge-related disordersOther
05

Safety considerations

On-target toxicity (removal of beneficial or transiently senescent cells critical for tissue repair or wound healing)Immune-related effects (excessive or misdirected immune activation)Potential tissue dysfunction if non-pathological senescent cells are depleted
06

Interacting drugs

Dasatinib

15 more in the full profile.

07

Biomarkers

p16^INK4a^p21^CIP1/WAF1^SA-β-galactosidase (SA-β-gal)Urokinase-type plasminogen activator receptor (uPAR)Glycoprotein nonmetastatic melanoma protein B (GPNMB)Dipeptidyl peptidase 4 (DPP4)CD9CD24NOTCH receptorsB2MSASP component profile

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