Satomi Miwa

TL;DR: Observations suggest a hypothesis for the main, ancestral function of uncoupling proteins: to cause mild uncoupled and so diminish mitochondrial superoxide production, hence protecting against disease and oxidative damage at the expense of a small loss of energy.

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.

TL;DR: It is demonstrated that cellular senescence drives hepatic Steatosis and elimination of senescent cells may be a novel therapeutic strategy to reduce steatosis.

TL;DR: The results suggest that mitochondria are a candidate target for interventions to reduce the deleterious impact of senescence in ageing tissues.

TL;DR: Evidence is shown that dysfunctional telomeres and/or accumulated DNA damage can induce a DNA damage response leading to a phenotype in postmitotic neurons that resembles cell senescence in multiple features, and it is concluded that aSenescence-like phenotype is possibly not restricted to proliferation-competent cells.