Mitochondria and chronic effects of cancer therapeutics: The clinical implications.

摘要: One of the major mechanisms action chemo-radiation is to induce cellular senescence, which exerts crucial roles in age-related pathology. The concept senescence evolved, and novel understanding senescence-associated reprogramming/stemness has emerged. This new emphasizes as not only cell cycle arrest but describes that subsets senescent cells induced by chemotherapy can re-enter cycles, proliferate rapidly, acquire “stemness” status. Cancer therapeutics, including triggers toxicity effects through damaging mitochondria, primarily upregulation mtROS production leading subsequent mtDNA telomeric DNA damage elicitng responses (DDR). ultimate goal this review highlight stemness that cancer treatment its adverse on vascular system. We will describe how simultaneously producing reactive oxygen species mitochondria promoting DDR nucleus. discuss potential clinical targeting poly (ADP-ribose) polymerase might prevent downstream mitochondrial dysfunction confer protection survivors. Overall we emphasize importance recognizing consequences cardio-toxic several treatments therefore developing personalized therapeutic approaches screen for inflammatory cardiac testing better patient survival.