Judith Campisi

The paper identifies senescent fibroblast heterogeneity in IPF and links it to DNA damage response dysregulation using gene expression analysis.

This study shows DNA damage in neurons leads to a senescent-like state similar to Alzheimer's disease, with distinct features from fibroblasts.

This study shows that overexpressing an Alu transposon in human fibroblasts causes widespread disruptions in aging-related pathways across transcriptome, proteome, and secretome.

This study shows that cellular senescence contributes to Doxorubicin-induced vascular endothelial dysfunction and that senolytic treatment can prevent this dysfunction.

This study identifies functionally distinct senescent cell subpopulations based on cell cycle status, showing G2-arrested cells secrete more IL-6 and are more sensitive to senolytic treatment.

This study shows that doxorubicin chemotherapy induces aortic stiffening via cellular senescence and the senescence-associated secretory phenotype, which can be mitigated by senolytic therapy.

This study identifies aging-associated proteomic and lipid signatures in exosomes from senescent cells and human plasma, revealing shared biomarkers and pathways linked to senescence and tissue damage.

The paper establishes a senotype of doxorubicin-induced senescence in postmenopausal human ovarian tissue using single nuclei sequencing and proteomics.

This study identifies apigenin as a senomorphic agent that modulates the senescence-associated secretory phenotype (SASP) to improve aging-related outcomes.

This study identifies ADAM19 as a modulator of the senescence-associated secretory phenotype (SASP) and shows that its inhibition reduces gut permeability and senescence markers in multiple species.

This study shows that substrate stiffness influences doxorubicin-induced senescence and secretory profiles in human pulmonary fibroblasts, with collagen enrichment observed in high-stiffness conditions.

This study shows that sleep disruption in mice increases cellular senescence in visceral adipose tissue, leading to oxidative stress and DNA damage, which may accelerate aging and age-related diseases.

This study uses single-cell whole-genome sequencing to compare mutation burdens in early passage and deeply senescent human fibroblasts, finding increased single-nucleotide variations and aneuploidies in senescent cells.

This study shows that senescent Schwann cells, induced by aging and chronic denervation, impair axonal regeneration by reducing c-Jun expression and secreting inhibitory factors, and that eliminating these cells improves regeneration.

This study uses single-nuclei multi-omics analysis to identify molecular and cellular changes in human ovarian ageing and links genetic variants to age at natural menopause.