Fig. 3

Prospective senotherapeutic strategies to subvert AMD progression. (1) Selective elimination or modulation of senescent cells through senolytics such as dasatinib + quercetin, inhibitors of Bcl-2 or BET proteins, chimeric antigen receptor (CAR) T cells, or by modulating neutrophil-induced NETosis, which can redirect immune responses against senescent cells. (2) Modulation of senescence-related signaling networks (senomorphics) to attenuate SASP through, for example, regulating NF-κB, mTOR, and AMPK pathways, or utilizing monoclonal antibodies against SASP factors, such as IL-6. (3) Inhibition of senescence in the eye using cell cycle regulators, p53/Rb sumoylation inhibitors, mitochondria-derived peptides, or lipid mediators. (4) Restoration of cholesterol homeostasis/flux and normal function of macrophages via liver X receptor (LXR) agonists or miR-33 inhibition, which has proved beneficial in the inhibition of retinal degeneration in vivo