Targeting the SASP: Inflammaging at the Interface of Senescence and Immunity

This Research Topic explores the bidirectional relationship between the Senescence-Associated Secretory Phenotype (SASP) and immune system aging. Cellular senescence is a physiological process, but the persistent accumulation of senescent cells with age leads to chronic secretion of pro-inflammatory cytokines, chemokines, and proteases - a phenomenon known as inflammaging. Critically, this relationship runs in both directions: the SASP actively drives immune dysfunction and exhaustion, while a declining immune system, in turn, loses its capacity to recognize and clear senescent cells, allowing them to accumulate further. This reciprocal, self-reinforcing loop is increasingly recognized as a central driver of age-related decline, yet the mechanisms sustaining it - and the points at which it can be interrupted - remain incompletely understood.This collection welcomes contributions examining both sides of this relationship: how the SASP shapes immune cell function and fate, and how immune aging permits or accelerates SASP accumulation. We invite submissions spanning basic mechanistic discovery, translational models, and clinical or population-based studies, across any tissue, organ system, or disease context where this crosstalk plays a role.We particularly encourage manuscripts on:- Molecular pathways governing SASP induction and its downstream effects on immune cell populations (innate and adaptive)- Mechanisms by which immune aging impairs surveillance and clearance of senescent cells- Tissue-specific senescence heterogeneity and its role in modulating the dynamic microenvironmental effects of the SASP- The dynamic regulation of the SASP as a key determinant of chronic low-grade inflammaging and systemic disease progression- Tissue- and organ-specific manifestations of this feedback loop (e.g., skin, vasculature, bone, brain, gut, metabolic tissues)- The contribution of this senescence-immunity loop to specific age-related diseases (cancer, cardiovascular, metabolic, neurodegenerative, or autoimmune conditions)- Biomarkers capturing SASP activity, immune decline, or their combined signature- Emerging strategies (pharmacological, immunological, or lifestyle-based) that interrupt or rebalance this feedback loop- Preclinical models and clinical or observational studies characterizing this bidirectional relationship over the aging trajectoryWe welcome studies from researchers across basic, translational, and clinical domains. Topic editors: Hanane CHAJRA, Pritam Biswas, Kalpna Durairaj, Jordan Plews, Koji Tanabe Source: https://www.frontiersin.org/research-topics/84074/targeting-the-sasp-inflammaging-at-the-interface-of-senescence-and-immunity