Telomeres, Telomerase, and Senescence

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

The paper identifies a telomere-specific mechanism for setting telomere length in yeast, showing that telomere-specific regulation depends on Sir4, Tbf1, and a telomerase recruitment pathway.

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 shows that nuclear actin and replication stress regulate telomerase recruitment to telomeres via ATR and mTOR, enabling telomere length maintenance in human cells.

The paper uses bulk and single-cell RNA sequencing to identify senescence-associated biomarkers in canine mesenchymal stem cells across passages.

The paper shows that reduced ATM signaling via ROS at physiological oxygen delays replicative senescence by inhibiting DDR activation.

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

This study shows that HIF-1α activation defines the SASP across different stressors, independent of micronuclei-induced cGAS/Sting activation.

This study shows that human fibroblasts from aged individuals exhibit chromosomal instability due to oxidative stress-induced replication stress, similar to findings in aged mouse fibroblasts.

This study shows that progranulin deficiency worsens age-related vascular damage in mice, affecting endothelial function and vascular remodeling.

This study uses multi-omics profiling to characterize senescent endothelial cells and their EVs, identifying molecular signatures and regulatory networks involved in vascular aging and CVD.

This study shows ZONAB regulates endothelial cell senescence by controlling DNA methylation and mitochondrial function, impacting angiogenesis and vascular health.

The paper identifies a first-in-class inhibitor of the TRF1-TIN2 protein-protein interaction using fragment screening and structural methods.

The paper shows CD4 T cells release telomere-rich vesicles called Rivers, which rejuvenate senescent tissues and extend lifespan in mice.

This study quantifies senescence burden at the single-cell level across tissues in mice and human PBMCs, revealing tissue-specific ageing dynamics and senescence marker heterogeneity.

TelOMpy measures individual telomere lengths from optical genome mapping data, showing high variation and diet-induced shortening in mice.

The paper identifies TERRA promoters in subtelomeres and interstitial telomeric sequences, showing their transcriptional activity and contribution to TERRA RNA production.

The paper quantifies telomere content variation across 26 global human populations and finds significant differences between African-ancestry populations in the Americas and other superpopulations.

This study identifies senescent fibroblasts in lung cancer stroma that alter tumor metabolism and plasticity, and shows that targeting these cells with XL888 reduces tumor burden.

This study identifies senescent cells as resembling developmental signaling centers by showing their SASP activates conserved developmental pathways across species.

The paper identifies Eda2r as a key mediator in both developmental and pathological senescence by profiling senescent cells in mouse limb development and comparing them to in vitro and in vivo models.

SAMP-Score identifies pro-senescence compounds in Sen-Mark+ cancers by classifying senescence based on morphology, leading to the discovery of QM5928.

This study shows that restoring FOXM1 activity in aged cells reduces DNA damage and epigenetic changes, inhibiting senescence enhancers and offering a therapeutic approach to aging.

The paper examines p21Cip1 and p16Ink4a expression in senescent cells across tissues, revealing heterogeneity and tissue-specific SASP profiles.

This study shows that telomerase deficiency in zebrafish accelerates brain ageing by promoting senescence, inflammation, and blood-brain barrier dysfunction.

The paper shows senescent human fibroblasts increase FasL expression, leading to T and NK cell apoptosis and impaired tumor immune response in humanized models.

This study shows that doxorubicin-induced senescent RPE-1 cells exhibit unbounded growth and proteome imbalance, revealing dynamic regulatory mechanisms rather than passive arrest.

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

The paper assesses fin tissue as a non-lethal surrogate for measuring telomere length and DNA methylation in gonads of turquoise killifish, showing strong correlation with age-related changes.

This study shows that telomere length is maintained in telomerase-deficient zebrafish during caudal fin regeneration via the ALT pathway, suggesting its role in supporting high cell proliferation rates.