1 Introduction The development of numerous diseases and organismal aging are primarily driven by increased cellular senescence [1-3]. A permanent state of cell cycle arrest and a variety of phenotypic alterations, especially the senescence-associated secretory phenotype (SASP), are hallmarks of cellular senescence [1, 4]. SASP impairs the normal regenerative capacity of tissues and triggers the deterioration of tissue function [4]. Biological aging is accelerated by environmental exposure [5].
