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@aging-us.bsky.socialOct 13, 2026, 10:00 PM

πŸ”† #PaperSpotlight:
A new #Research paper was published on September 16, titled β€œTargeting phospholipase Pla2g15 reduces long-chain BMP phospholipids abundance and senescence in kidney cells.”

πŸ”— https://bit.ly/4hMI0G8

#Aging #Quote #CellularSenescence #Kidneys #PeerReviewed

@aging-us.bsky.socialOct 13, 2026, 6:00 PM

πŸŽ₯ #AgingShort:
Abstract #Video of the #Research paper "Targeting phospholipase Pla2g15 reduces long-chain BMP phospholipids abundance and senescence in kidney cells.”

πŸ”— https://doi.org/10.18632/aging.206415

#Aging #PaperSpotlight #CellularSenescence #Kidneys #CKD #Mitochondria #OA

@aging-us.bsky.socialOct 13, 2026, 4:00 PM

πŸ”† #PaperSpotlight:
The #Research paper "Targeting phospholipase Pla2g15 reduces long-chain BMP phospholipids abundance and senescence in kidney cells" was recently published in Volume 18.

#PressRelease ⬇️
https://bit.ly/4yL76fP

#Aging #CellularSenescence #Kidneys #OA #Press

@sigtrans-sttt.bsky.socialOct 13, 2026, 9:08 AM

This study shows that #eccDNA-derived circular MIR144 drives age-related #CardiacRemodeling by inducing cardiomyocyte senescence and by promoting interstitial fibrosis and systolic dysfunction in mice.

#STTT #OpenAccess: doi.org/10.1038/s413...

#CardiacFibrosis #CellularSenescence

Circular MIR144 from eccDNA is a superior senescence agonist in aging hearts
@aging-us.bsky.socialSep 29, 2026, 10:00 PM

πŸ”† #PaperSpotlight:
A new #Review was published on September 8, titled β€œDevelopmental senescence misregulation in congenital disorders: CHARGE syndrome as a candidate model.” @usc.gal

πŸ”— https://bit.ly/47u1xX6

#Aging #Quote #CellularSenescence #Genetics #Longevity #OA #PeerReviewed #Publishing

@aging-us.bsky.socialSep 29, 2026, 8:00 PM

🎧 Listen to our #PressRelease on the #Review "Developmental senescence misregulation in congenital disorders: CHARGE syndrome as a candidate model."

https://bit.ly/3TV7mKc

#Aging #Podcast #Audio #SoundCloud #PaperSpotlight #CellularSenescence #OA #Publishing #MedEd #Press

@aging-us.bsky.socialSep 29, 2026, 6:00 PM

πŸŽ₯ #AgingShort:
Abstract #Video about the #Review, titled "Developmental senescence misregulation in congenital disorders: CHARGE syndrome as a candidate model.” @usc.gal

πŸ”— https://bit.ly/47u1xX6

#Aging #PaperSpotlight #CellularSenescence #Genetics #Longevity #OA #PeerReviewed #Publishing

@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 β€” principally IL-6, IL-8, and other NF-ΞΊB-dependent secreted factors β€” 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.
@jthoracdis.bsky.socialSep 10, 2026, 8:11 AM

πŸ”¬ COPD lungs may age 10-20 years faster due to oxidative stress. With no current drugs targeting the COPD inflammatory pattern, Prof. Barnes highlighted #senolytics (like Bcl-xL inhibitors) as potential therapies to clear senescent cells. πŸ’Š #RespiratoryMedicine #CellularSenescence

@jthoracdis.bsky.socialSep 10, 2026, 7:46 AM

πŸ”¬ COPD lungs may age 10-20 years faster due to oxidative stress. With no current drugs targeting the COPD inflammatory pattern, Prof. Barnes highlighted #senolytics (like Bcl-xL inhibitors) as potential therapies to clear senescent cells. πŸ’Š #RespiratoryMedicine #CellularSenescence