Telomere Shortening as Biological Hallmark of Cellular Senescence and Longevity-An Update
The process of ageing is the consequence of both genetic and epigenetic alterations associated with metabolic disorders and characterized by mitochondrial dysfunctions generated due to reactive oxygen species. Current reports indicate that cellular ageing or senescence retrograde mitochondrial signaling disorders, telomere shortening, heterochromatin configuration, endoplasmic reticulum strain and unfolded protein responses. Supplemental vitamins, inhibition of cell cycle arrest and controlled expressions of tumor promoting genes p53, p21CIP1 and p16INK4a are robust telomere length longevity promoting interventions and prolong youthful cell functions. This review is aimed to provide an update on the molecular approach mediating the cellular ageing in developmental and programmed replicative ageing cascade with focus on DNA damage response in various cell types. Through rational ideas and critical investigation, we conclude that the combination of irretrievable alternations caused by metabolic reactions elicit the accelerated mechanisms of cellular ageing.