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@mitoworld.bsky.socialOct 5, 2026, 9:35 PM

Check out the MitoBlog Q&A w/ authors of @nature.com paper: #Mitochondrialmetabolism & epigenetic crosstalk drive #SASP. Peter Adams & Joao Passos reveal a new #mitochondria #senescence #inflammaging pathway.

mitoworld.org/mitochondria...

#mitoscientists #mitochondrialdisease #UMDF

@alicefrolov.bsky.socialSep 18, 2026, 5:01 PM

Cell-fate partitioning after senescence induction: modeling SASP-driven escape trajectories

#CellularSenescence #SASP #CellCycleReentry #SenescenceEscape #TumorSuppression #NFkBSignaling #SystemsBiology #ComputationalCellBiology

Cell-fate partitioning after senescence induction: modeling SASP-driven escape trajectories I am sharing a data visualization that formalizes an increasingly discussed but underappreciated phenomenon in the senescence literature: the capacity of a subpopulation of arrested cells to re-enter the cell cycle rather than remaining stably arrested or undergoing clearance. The figure, titled "Cell-fate partitioning after senescence induction," uses a bidirectional flow trajectory (streamgraph-style stacked area) to render the temporal redistribution of an initial senescent-induced cohort across three terminal or quasi-terminal states over a 30-day window: stable arrest, apoptotic clearance, and senescence escape. The subtitle emphasizes that these are simulated dynamics, not empirical measurements; the parameterization is literature-grounded, calibrated to reported ranges for p16INK4a/p21CIP1 durability, SASP factor accumulation kinetics, and escape frequencies observed in oncogene- and therapy-induced senescence models. The streamgraph format is deliberate. Because escape is a flux phenomenon rather than a static endpoint, the bidirectional banding captures net transitions between compartments, including the small but non-negligible reflux from a metastable arrested state back into proliferation. The simulation encodes a positive-feedback term whereby paracrine and autocrine SASP components — principally IL-6, IL-8, and other NF-κB-dependent secreted factors — lower the effective barrier to CDK reactivation in cells with attenuated tumor-suppressor signaling. The escape band consequently widens after the SASP matures, roughly days 8 to 15 in this parameterization, consistent with the delayed secretory phenotype. I would welcome critique on the transition-rate assumptions, particularly the coupling coefficient between SASP intensity and escape probability, which remains poorly constrained empirically.
@bbparis1984.bsky.socialSep 8, 2026, 10:28 PM

However, against our prediction, #L1 expression did NOT simply make healthy fibroblasts look aged or senescent.
In fact, many transcriptional effects were broadly opposite to signatures of #aging, #senescence (including repression of #SenMayo and #SASP). 4/7