A New Pathway for Senescence Regulation

Research concerning senescence has become a hotspot since the conception of ‘cellular senescence’ was put forward by Drs. Hayflick and Moorhead over five decades ago [1]. Recently, a paper published in Science by Kang and colleagues, which this article aims to comment on, provides evidence of a new pathway involved in senescence [2]. Senescence is a physiological and pathological process induced by numerous factors, during which cell growth ceases and gene expression alters. As can be imagined, such state protects against the development of cancer and plays an important role in tissue repair [3]. On the other hand, senescence is involved in many other processes such as aging and neurodegenerative disease [4], [5], [6]. Recent studies show that senescent cells produce senescence-associated secretory phenotype (SASP) factors including chemokines, proteases, pro-inflammatory cytokines, growth factors, macrophage inflammatory proteins (MIPs), and granulocyte–macrophage colony-stimulating factors (GM-CSFs) [7], [8]. It is known that SASP is mediated by the transcription factors NF-κB [9]. But how SASP is initiated and maintained is not clear.