Behind a paywall
Abstract
Chronic inflammation often causes tissue fibrosis. This state is characterized by the accumulation of activated fibroblasts—cells that switch to an active state to help repair tissue—and by excessive collagen deposition and an environment that suppresses immune activity (1). Senescent cells, a type of nonproliferating cells that secrete bioactive molecules, can support tissue repair after injury. However, their persistence worsens inflammation, which increases fibrosis and leads to organ decline (2). Senescent cells also accumulate in the tumor microenvironment, where they promote immune suppression (3, 4). Killing senescent cells could counteract their negative effects. However, senolytic drugs are toxic to the entire body, which limits their clinical potential (5–7). On page 1313 in this issue, Hinterleitner et al. (8) report that senescence-modulating nanoparticles can selectively deliver drugs to a subset of senescent cells. This targeted approach remodels the microenvironment of fibrotic tumors and makes them responsive to immunotherapy.
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