Cellular senescence is a stable cell cycle exit that is believed to halt proliferation of damaged cells, thus representing a potential barrier against cancer progression. Conversely, senescence was recently shown to contribute to the detrimental phenotypes associated with aging. How to reconcile the positive effect of senescence early in life with its detrimental impact in aged organisms remains elusive. One hallmark of all senescent cells is their unique ability to secrete a discrete yet heterogeneous set of cytokines, chemokines and metalloproteases collectively referred to as the Senescence Associated Secretory Phenotype (SASP). The exact contribution of the SASP to the diverse phenotypes elicited upon activation of the senescence pathway remains largely unknown.

The overarching goal of this Research Topic is to begin to understand how the secretion of the SASP contributes to the diverse phenotypes driven by the presence of senescent cells both in healthy aging and in diseases situations. As novel technologies allow the identification of expressed and secreted factors at the single cell level, recognizing the context- and cell-specific range of the SASP becomes possible. Additionally, the generation of in vivo and ex vivo models that faithfully recapitulate the gamut of cells, including immune cells, present in a given organ or tissue, now allows the determination of the impact of the SASP on a complex network of cellular interactions. By combining these approaches, it becomes possible to understand how the SASP affects normal and pathological conditions both at the molecular and the cellular levels.

We welcome the submission of review and original research articles that cover the following aspects, but are not limited to:

• Molecular events leading to the activation of a secretory phenotype in senescent cells
• Heterogeneity of the SASP among senescent cells, based either on the cell of origin or the inducer of senescence.
• Paracrine versus autocrine effects of the SASP
• Impact of the SASP on immune cells recruitment, activation and elimination in normal contexts, disease and aging
• Contribution of individual SASP factors to the "inflamm-aging"
• Identification of non-protein SASP factor

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Frontiers in Aging

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