Anat Biran

TL;DR: The finding that senescent cells can be eliminated pharmacologically paves the way to new strategies for the treatment of age-related pathologies.

TL;DR: It is shown that perforin deficient mice accumulate more senescent cells and have a shorter lifespan, and that this phenotype can be reversed with administration of a senolytic drug.

TL;DR: A new way to precisely quantify and identify senescent cells in tissues on a single‐cell basis is presented, enabling a deeper understanding of the senescent state in vivo and paves the way for screening of senescence cells for identification of newsenescence biomarkers, genes that bypass senescences or senolytic compounds that eliminate senescent Cells.

TL;DR: Fusion-inducedsenescence might be needed for proper syncytiotrophoblast function during embryonic development, and reuse of this senescence program later in life protects against pathological expression of endogenous fusogens and fusogenic viral infections.

TL;DR: It is shown that granule exocytosis, but not death-receptor-mediated apoptosis, is required for NK-cell-mediated killing of senescent cells, and this results provide new insights into the immune surveillance of senescence and reveal how granuleExocytotic has a protective role against liver fibrosis.