HoldsUp

Judith Campisi

Buck Institute for Research on Aging

Judith Campisi, Ph.D., is a professor of biogerontology at the Buck Institute for Research on Aging and a co-editor in chief of the journal Aging. Her research focuses on cellular senescence and its roles in the aging process and cancer development. Her published studies investigate mechanisms such as DNA damage, the senescence-associated secretory phenotype (SASP), senotherapeutic strategies, and the impact of senescent cells across various tissues and age-related conditions.

32 claims checked on air: 4 context 2 overstated 25 supported 1 unverified 2 flagged

What they said on air - citing their own research

2 citing their own research

0:10:20supportedvery lowtheir own paperJudith Campisi, Ph.D. on Cellular Senescence, Mitochondrial

Senescent cells secrete bioactive lipids, specifically prostaglandins and leukotrienes, which modulate inflammation, fibrosis, and tissue repair.

"And they also now, we know very new data from our lab, they secrete um bioactive lipids like prostaglandins and leukotrienes, which are very important for modulating inflammation, fibrosis, but also again tissue repair." (said at 0:10:20)

Preclinical in vitro and animal studies demonstrate that senescent cells secrete bioactive lipid mediators as part of the senescence-associated secretory phenotype (SASP), specifically leukotrienes and prostaglandins. These bioactive eicosanoids play active functional roles in modulating local inflammation, promoting or limiting tissue fibrosis, and participating in wound healing and tissue repair. Because the available evidence is derived from cell culture experiments and animal models, the GRADE certainty is very low.

0:23:39supportedvery lowtheir own paperJudith Campisi, Ph.D. on Cellular Senescence, Mitochondrial

When astrocytes become senescent, they become less effective at protecting neurons from neurotoxins such as neurotransmitter toxicity.

"And we even have new evidence that astrocytes, as you know, help protect the neurons from certain types of toxicity like neurotransmitter toxicity. And we can show that when astrocytes become senescent, they become less effective in that protective response." (said at 0:23:39)

Preclinical in vitro research supports the claim. Astrocytes normally clear excess neurotransmitters such as glutamate from the synaptic cleft to prevent excitotoxicity. When primary human astrocytes undergo senescence, the expression of glutamate and potassium transporters is significantly downregulated, leading to impaired glutamate clearance and increased neuronal death in co-culture models. Because this evidence is derived from in vitro and preclinical mechanistic models, certainty is graded as very low.

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