Telomeres, Telomerase, and Senescence

This study characterizes replicative senescence in primary human astrocytes, identifying molecular features and L1HS retrotransposon activation associated with senescence.

This study establishes a human in vitro model of DNA damage-induced senescence in neural progenitor cells and identifies senescence-associated transcriptomic and functional changes linked to hippocampal ageing and neurodegeneration.

This study uses long-read sequencing to show that telomere length differences between chromosome arms influence structural genome changes in IDH-mutant astrocytomas.

The paper analyzes transcriptomic changes in human fibroblasts under different senescence-inducing conditions, finding shared pathway-level responses and inducer-specific gene-level variations.

This study shows that a H2A.Z mutant reduces the senescence-associated secretory phenotype in human fibroblasts without affecting cell cycle genes.

This study maps age-related cellular senescence in human lymph nodes, identifying senescence markers and spatial shifts in germinal center B cells.

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 extracellular vesicles from senescent tumor cells are both necessary and sufficient to induce paracrine senescence in neighboring cells.

The paper identifies senescence-associated enhancer RNAs (SAeRs) and shows their functional role in linking chromatin reprogramming to post-transcriptional regulation of senescence.

This study shows that chronic HBV infection causes CD4 T-cell senescence with DNA damage and telomere erosion, while the MRN-ATM pathway is activated as a compensatory mechanism to maintain T-cell function.

This study shows that RasG12V-induced epithelial senescence in Drosophila triggers host metabolic syndrome through cytokine signaling, linking oncogene-induced senescence to metabolic disorders.

The paper develops a BRET assay to measure telomere length in S. cerevisiae by correlating BRET ratios with telomere length data from long-read sequencing.

The paper develops a data-analysis pipeline for HT-SELEX datasets to study DNA-binding properties of telomeric proteins, showing binding preferences for G-enriched sequences and secondary structures.

This study shows that transplanting ANXA1-negative CD8 naive T cells extends lifespan and improves health in aged mice by reducing senescence.

This study shows BAP1 loss drives senescence in uveal melanoma and makes tumors more responsive to senolytics and radiation.

The paper identifies a distinct p16INK4a-associated senescence signature in human ovarian tissue through proteogenomic profiling and spatial analysis.

The paper identifies TRFL7 as a telomere-binding protein in Arabidopsis, showing it functions similarly to human TRF2 in telomere maintenance.

This paper validates the reproducibility and utility of the p16-3MR mouse model for studying senescent cells across various conditions and discusses its strengths and limitations.

The paper develops a machine learning classifier to identify cellular senescence using single-cell RNA-seq data, finding it outperforms marker-based approaches and reveals new mechanistic insights.

This study identifies soluble DLK1 from senescent microglia as a factor impairing oligodendrocyte function and altering neuronal activity in aging.

This study shows genetic and chemical partial reprogramming targets senescent cells to reduce aging-related inflammation and improve mitochondrial function in aged mice without restoring proliferation.

This study shows that targeting GD3 ganglioside, a senescence-associated immune checkpoint, improves healthspan and reduces age-related diseases with sex-specific benefits in mice.

The paper identifies structural variations in TP53 that inactivate TCAB1, a telomerase chaperone, and show these variations are prevalent in ALT-positive osteosarcoma tumors.

This study identifies senescent CD8+ T effector memory cells as functionally impaired and enriched in aging and disease, and shows they hinder immunotherapy responses.

This study shows senescent cells release chromatin components via extracellular particles, activating inflammation in neighboring cells and being present in aged mice.

This study uses Nanopore whole-genome sequencing to show conserved chromosome-specific telomere length patterns across tissues and populations, revealing coordinated regulation and potential disease risk factors.

This study shows that p16INK4A-expressing fibroblasts release small extracellular vesicles that induce paracrine senescence in neighboring cells.

This study identifies SLFN11 as a suppressor of the ALT telomere maintenance pathway, showing its re-expression reduces ALT activity in cancer cells.

The paper identifies and maps senescent cells in postmenopausal ovaries using p16 expression and spatial transcriptomics, revealing a fibro-inflammatory signature associated with aging.

The paper identifies a subset of senescent cells marked by surface ATP6V1B2 that exhibit increased resistance to apoptosis and are associated with DNA repair.