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Optispan Podcast with Dr. Matt Kaeberlein

Released April 11, 2024

Key References


Baker DJ, Wijshake T, Tchkonia T, et al. Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders. Nature. 2011;479(7372):232-236

Demonstrated a causal link between cellular senescence and aging phenotypes. Removal of p16+ senescent cells delayed onset of aging-related phenotypes in skeletal muscle, adipose, and eye.

Xu M, Pirtskhalava T, Farr JN, et al. Senolytics improve physical function and increase lifespan in old age. Nat Med. 2018;24(8):1246-1256

Mice can be prematurely aged via senescent cell transplant.  Effects can be reversed with senolytic therapy

Baker DJ, Childs BG, Durik M, et al. Naturally occurring p16 Ink4a-positive cells shorten healthy lifespan. Nature. 2016;530(7589):184-189

Selective elimination of p16+ senescent cells extended median lifespan in mice by ~25% and attenuated age-related deterioration of kidney, heart and fat.

Yousefzadeh MJ, Flores RR, Zhu Y, et al. An aged immune system drives senescence and ageing of solid organs. Nature. 2021;594(7861):100-105

When induced in immune cells alone, cellular senescence is propagated throughout the body and senescent cells are found in different cell and tissue types. Rapamycin decreased cellular senescence and improved immune function


Liu Y, Sanoff HK, Cho H, et al. Expression of p16(INK4a) in peripheral blood T-cells is a biomarker of human aging. Aging Cell. 2009;8(4):439-448

Seminal paper showing that p16 measured in human blood is a biomarker of aging with potential clinical utility

Smitherman AB, Wood WA, Mitin N, et al. Accelerated aging among childhood, adolescent, and young adult cancer survivors is evidenced by increased expression of p16INK4a and frailty. Cancer. 2020:1-9

Cellular senescence increased in patients receiving chemotherapy and senescent cell burden remained elevated years into survivorship. The increase correlated with treatment intensity and early-onset aging phenotypes in young adults who survived childhood cancers

Tsygankov D, Liu Y, Sanoff HK, Sharpless NE, Elston TC. A quantitative model for age-dependent expression of the p16INK4a tumor suppressor. Proc Natl Acad Sci U S A. 2009;106(39):16562-16567

Computational modeling of the dynamics of p16+ cellular senescence in healthy donors.  Model revealed rate of p16 accumulation with chronological and lifestyle factors such as smoking and exercise habits

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