Kurt O. Johnson

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: The hypothesis‐driven, bioinformatics‐based approach used to discover that dasatinib (D) and quercetin (Q) are senolytic can be extended to increase the repertoire ofsenolytic drugs, including additional cell type‐specific senolytics agents.

TL;DR: It is found that senescent fat progenitor cells accumulate in adipose tissue with aging and acquire a senescence-associated secretory phenotype (SASP), with increased production of proinflammatory cytokines compared with nonsenescent cells.

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.