Figure 9.

A schematic model. In Cr(VI)-exposed L02 hepatocytes, dysfunction of mitochondria made accumulation of the intracellular ROS contributing to subsequent Ca²⁺overload in cytoplasm/mitochondria and activation of NF-κB signaling. In addition, NF-κB, a transcription factor of inflammatory factors [52], is activated by Ca²⁺overload and then elevates the expression and secretion of inflammatory factors, inducing premature cellular senescence. Furthermore, SASP may lead to senescence-related inflammation, metabolic dysregulation, stem cell dysfunction, aging phenotypes, and liver diseases [53].