Telomere biology represents an emerging focal point in aging research, specifically in the context of inflammation and cellular senescence. Telomeres serve as protective caps at chromosome ends and ensure genomic stability; however, their progressive shortening during replicative cycles, or dysfunction through external stressors, is intrinsically linked to cellular fate decisions. Increasing evidence highlights a bidirectional relationship: telomere attrition can trigger DNA damage signaling pathways that initiate senescence and the establishment of a senescence-associated secretory phenotype (SASP). This, in turn, amplifies local and systemic inflammation. Meanwhile, chronic inflammatory states and oxidative stress accelerate telomere erosion, further propagating cellular and tissue dysfunction. Despite advances in delineating these connections, substantive questions remain regarding the molecular mechanisms governing telomere-induced inflammation and senescence in vivo, tissue- and disease-specific features of this nexus, and optimal strategies to mitigate its pathological consequences.

This Research Topic aims to elucidate the mechanistic and functional interplay between telomeres, inflammation, and senescence in human aging and disease. Central goals include deciphering how specific telomeric lesions differentially induce senescence and modulate SASP composition, unraveling the pathways by which inflammatory signaling exacerbates telomere damage, and delineating the feedback loops underpinning this interaction in diverse cell types and tissues. The overarching objective is to define actionable biomarkers and therapeutic targets that could disrupt the pathological cycle linking telomere dysfunction with chronic inflammation and tissue decline, and to apply this understanding towards translational interventions in age-related diseases.

To gather further insights into the boundaries and drivers of the telomere-inflammation-senescence axis, we welcome articles addressing, but not limited to, the following themes:

o Mechanisms by which telomere dysfunction modulates senescence signaling and SASP output in different cellular contexts
o Bidirectional influences between inflammatory pathways (e.g., NF-κB, cGAS–STING) and telomere maintenance mechanisms
o Tissue- and disease-specific mapping of telomere–inflammation crosstalk across aging and lifespan
o Identification and validation of telomere-inflammation biomarkers in human cohorts and clinical samples
o Experimental approaches to target telomere attrition, senescence, or inflammatory signaling for disease modification
o Advances in omics, single-cell systems, and animal models to dissect causality in telomere-driven inflammaging
o Translational perspectives on risk stratification, therapy development, and clinical outcome prediction based on telomere-inflammation signatures

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Telomeres at the Nexus of Inflammation and Senescence