Finding. Human HMC3 microglia senesce two ways. Jose, Platt and colleagues hit them with doxorubicin or chronic high glucose. Both swell, turn SA-beta-gal on, lose metabolic viability, and light p53-p21 with leftover DNA-damage signaling. Glucose also raises p16 and sends p21 to the nuclear edge. Mitochondria disagree. Doxorubicin turns NRF2-TFAM down. Glucose turns that axis on and raises KEAP1, an antioxidant push that still does not put mitochondrial content back.
Score 74. Stressor-split mitochondrial biogenesis in microglial senescence. Medium confidence: line, truncated abstract.