This #STTT study shows that disrupting aberrant glycolytic interactions eliminates #SenescentCells and alleviates #Aging-related dysfunctions, highlighting metabolic targeting to counteract #Senescence and age-associated pathologies.
#OpenAccess: doi.org/10.1038/s413...
PGAM1-Chk1-HIF-2α signaling axis activates FoxM1 to drive metabolic reprogramming & survival in #SenescentCells, showing that pharmacological disruption of the PGAM1-Chk1 interaction acts as a targeted #Senolytic to eliminate these cells.
#OpenAccess: doi.org/10.1038/s413...
#Senescentcells play a decisive role in tumor proliferation, according to a preclinical study led by Hospital del Mar Research Institute and @vhio.bsky.social
The findings open the door to a new combination of treatments
www.researchmar.net/news/791/res...
@hospitaldelmar.bsky.social
#mwgic #2025 #Aging #Longevity #Senescence #SenescentCells
www.sciencedaily.com/releases/202...
A lactate-driven PGAM1–Chk1 interaction sustains #glycolytic reprogramming and #DNARepair in #SenescentCells via HIF-2α/FoxM1 signaling; disrupting this axis induces #senolysis, improves #aging phenotypes, and reduces #LungFibrosis.
#OpenAccess in #STTT: doi.org/10.1038/s413...
The NIH-funded San Diego @NathanShockCenters.org brought scientists together for the first of two aging meetings, covering breakthroughs in #aging, #breastcancer, #senescentcells, #autophagy, and cellular identity. Read more: vist.ly/3mysxen
Scientists at Sanford Burnham Prebys and collaborators published findings in Nature Communications showing that mitochondria control a DNA repair protein's ability to suppress inflammation in #senescentcells, suggesting a potential treatment for healthier aging. More: vist.ly/3mxd3z9
FANCL establishes senescent cell quantification and reveals Agrimonia pilosa’s anti-aging effects. A breakthrough in longevity research. #FANCL #SenescentCells #AgrimoniaPilosa #Agrimoniin #AntiAging #CosmeticsIndustryInnovation
kokusaishogyo-online.jp/2025/03/182771
Protein That Reverses Aging
www.linkedin.com/pulse/protei...
#science #aging #antiaging #sanjanagajbhiye #PirawanChantachotikal #senescence #senescentcells #ap2a1 #research #Researcher #ResearchAndDevelopment #researchstudy #ResearchMatters #osteoporosis #earthcom #nationalgeographic
4/13 The culprit? Senescence. Cells stop dividing but refuse to die, becoming "zombie cells." They drive aging by accumulating damage and releasing inflammatory molecules (SASP). #SenescentCells #ZombieCells #Inflammation
Senescent cells. Image credit: Nabora Reyes/Peng Lab, UCSF
This lock stops the immune system from detecting and eliminating these cells, allowing them to resist treatment. This contrasts with #SenescentCells, which are highly inflammatory and use different mechanisms to evade the immune response.