Megan M. Weivoda

TL;DR: It is demonstrated that transplanting relatively small numbers of senescent cells into young mice is sufficient to cause persistent physical dysfunction, as well as to spread cellular senescence to host tissues, and a senolytic can reverse this dysfunction and potently increase lifespan in aged mice.

TL;DR: A causal role for senescent cells in bone loss with aging is established, and targeting these cells has both anti-resorptive and anabolic effects on bone, which suggests a novel treatment strategy not only for osteoporosis, but also for multiple age-related comorbidities.

TL;DR: This study indicates targeting senescent cells or their products may alleviate age-related dysfunction of progenitors, adipose tissue, and metabolism.

TL;DR: It is shown that reducing senescent cell burden in obese mice, either by activating drug‐inducible “suicide” genes driven by the p16Ink4a promoter or by treatment with senolytic agents, alleviates metabolic and adipose tissue dysfunction and that emerging senolytics agents hold promise for treating obesity‐related metabolic dysfunction and its complications.

TL;DR: Data show that with aging, a subset of cells of various lineages within the bone microenvironment become senescent, although senescent myeloid cells and senescent osteocytes predominantly develop the senescence‐associated secretory phenotype.