Pathological angiogenesis in retinopathy engages cellular senescence and is amenable to therapeutic elimination via BCL-xL inhibition - Crespo-Garcia, Sergio; Tsuruda, Pamela R.; Dejda, Agnieszka; Ryan, Rathi D.; Fournier, Frederik; Chaney, Shawnta Y.; Pilon, Frederique; Dogan, Taner; Cagnone, Gael; Patel, Priyanka; Buscarlet, Manuel; Dasgupta, Sonali; et al. (Cell metabolism, 2021)
Keywords: aging; angiogenesis; Animals; Apoptosis - drug effects; bcl-X Protein - antagonists & inhibitors; bcl-X Protein - metabolism; BCL-xL; cellular senescence; Cellular Senescence - drug effects; Collagen Type I, alpha 1 Chain - metabolism; Cyclin-Dependent Kinase Inhibitor p16 - deficiency; Cyclin-Dependent Kinase Inhibitor p16 - genetics; Cyclin-Dependent Kinase Inhibitor p16 - metabolism; diabetes; Disease Models, Animal; Endothelial Cells - cytology; Endothelial Cells - metabolism; Female; Flavonols - chemistry; Flavonols - pharmacology; Flavonols - therapeutic use; Humans; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Neovascularization, Pathologic; p16INK4A; retina; Retinal Diseases - drug therapy; Retinal Diseases - metabolism; Retinal Diseases - pathology; retinopathy; senolytic; Tacrolimus - analogs & derivatives; Tacrolimus - pharmacology; UBX1967; cellular senescence; UBX1967; retinopathy; BCL-xL; retina; angiogenesis; senolytic; aging; p16INK4A; diabetes; p16(INK4A)