Figure 4 Senotherapeutic targeting strategies

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Figure 4 Senotherapeutic targeting strategies Figure 4 | Senotherapeutic targeting strategies. Pro-senescence interventions such as cyclin-dependent kinase (CDK) 4 and CDK6 inhibition act on senescence-inducing pathways. Anti-senescence strategies include prevention, cell lysis and modulation of the senescence-associated secretory phenotype (SASP). Senescence prevention is achieved by mitigating pro-senescent stressors. Several drugs and lifestyle interventions currently considered life extending, such as caloric restriction, fall into this category. Senescent cells can be removed by senolysis by interfering with the anti-apoptotic and pro-survival signalling. Navitoclax, an inhibitor of BCL-2, BCL-xL and BCL-W, selectively induces apoptosis in senescent cells in vitro and in vivo. Besides removal, SASP modulation through inhibition of proinflammatory pathways such as NFκ-B, p38-MAPK, MAPKAPK2 is another option to interfere with senescent cells. This strategy includes inhibition of proinflammatory pathways or gene expression of SASP factors via bromodomain-containing protein 4 (BRD4) inhibition. RAAS, renin–angiotensin–aldosterone system; iBET, Bromodomain and extra-terminal motif inhibitor; JQ1, potent inhibitor of the BET family. Sturmlechner, I. et al. (2016) Cellular senescence in renal ageing and disease Nat. Rev. Nephrol. doi:10.1038/nrneph.2016.183