Circulating cell type senescence signatures track distinct dimensions of health status and trajectories in human longitudinal cohorts

Summary This study profiles cell-type-specific senescence signatures in circulating blood cells from human longitudinal cohorts and shows that these signatures track distinct dimensions of health status and aging trajectories. The findings establish circulating senescence signatures as high-resolution biomarkers of biological aging with potential utility for monitoring healthspan in humans.

SenCat: Redefining human cell senescence through multiomic profiling of multiple senescent primary cell types

Summary SenCat is a comprehensive multiomic atlas of human cell senescence generated by profiling multiple primary cell types induced to senescence through distinct triggers. Integrated analysis of transcriptome, epigenome, and proteome data across cell types and senescence inducers redefines the core features of the senescent state and identifies cell-type-specific and universal senescence signatures.

Senescence: An overlooked VSMC phenotype and therapeutic opportunity?

Summary This review examines the evidence for senescence in vascular smooth muscle cells (VSMCs) and its contribution to vascular aging and disease. The authors discuss the mechanisms driving VSMC senescence, its downstream consequences for vascular function, and the potential for senolytic and senomorphic interventions.

Viral Infection Induces Alzheimer's Disease-Related Pathways and Senescence in iPSC-Derived Neuronal Models

Summary Using iPSC-derived neurons and cerebral organoids, this study demonstrates that viral infections — including HSV-1 and tick-borne encephalitis virus — activate Alzheimer’s disease-related pathways and induce cellular senescence. The findings support a causal link between viral infection and neurodegeneration, suggesting that vaccination-based prevention of viral infections may reduce Alzheimer’s disease risk.

Senescence suppresses the integrated stress response and activates a stress-remodeled secretory phenotype

Summary This study reveals that senescent cells suppress the canonical integrated stress response (ISR) while activating a remodeled secretory program. The suppression of ISR in senescence is mechanistically linked to altered eIF2α phosphorylation dynamics, and the resulting secretory phenotype differs from the classical SASP, with implications for age-related tissue dysfunction.

Biology of Stress Responses in Aging

Summary This review covers the major cellular stress response pathways and how they are altered during aging. Topics include the integrated stress response, heat shock response, oxidative stress, proteostasis, and their connections to age-associated physiological decline and disease.