Thomas von Zglinicki

TL;DR: It is proposed that telomere-initiated senescence reflects a DNA damage checkpoint response that is activated with a direct contribution from dysfunctional telomeres.

TL;DR: It is suggested here that oxidative stress is an important modulator of telomeres loss and that telomere-driven replicative senescence is primarily a stress response.

TL;DR: A consensus from the International Cell Senescence Association (ICSA) is presented, defining and discussing key cellular and molecular features of senescence and offering recommendations on how to use them as biomarkers.

TL;DR: A hypothetical model in which cellular stress and preadipocyte overutilization with aging induce cellular senescence, leading to impaired adipogenesis, failure to sequester lipotoxic fatty acids, inflammatory cytokine and chemokine generation, and innate and adaptive immune response activation is proposed.

TL;DR: There exists a dynamic feedback loop that is triggered by a DNA damage response (DDR) and, which after a delay of several days, locks the cell into an actively maintained state of ‘deep’ cellular senescence, and is both necessary and sufficient for the stability of growth arrest during the establishment of the senescent phenotype.