Editorial: Cellular senescence in aging-related diseases: mechanisms and therapeutic targets

作者：Jie Zhou, Honghe Wang, Fangfang Zhu · 发表于：Frontiers in Cell and Developmental Biology · 年份：2026 · DOI：10.3389/fcell.2026.1835072 · 研究领域：Telomeres, Telomerase, and Senescence、Pluripotent Stem Cells Research、interferon and immune responses

The intricate interplay between cellular senescence and other fundamental biological processes is elegantly explored in several contributions. Ding et al present a comprehensive review examining the paradoxical relationship between senescence and cellular reprogramming. They demonstrate that senescent cells, through their SASP, can paradoxically enhance the reprogramming efficiency of neighboring cells via paracrine factors such as IL-6, while unsuccessful reprogramming attempts can trigger senescence as a failsafe mechanism. This bidirectional crosstalk has profound implications for both regenerative medicine and cancer therapy. The cellular mechanisms of senescent cell clearance are addressed in the original research by Funk et al, who demonstrate that NK cells efficiently recognize and eliminate senescent renal tubular epithelial cells through NKG2D receptor engagement with ligands H60b and Mult-1. This clearance is perforin-dependent and significantly impaired by the immunosuppressive drug cyclosporine A, providing mechanistic insights into why senescent cells accumulate under immunosuppressive conditions. Liu et al introduce an environmental dimension to senescence research, demonstrating how microplastics accelerate cellular aging through mitochondrial dysfunction, oxidative stress, and chronic inflammation, ultimately activating the cGAS-STING pathway and driving cellular senescence.The organ-specific consequences of cellular senescence are explored across multiple dis...