Cellular Senescence & Secretory Phenotypes through the lens of Ageing In Vivo Reprogramming Technology

Cellular senescence is a tumour-suppressing response that has recently been identified as a significant contribution to tissue ageing. Senescent cells fall into a persistent proliferative arrest which protects them against neoplastic transformation but they have a secretory phenotype which has long-term negative consequences. The effector mechanisms that underpin these senescence responses are currently being studied in order to discover therapeutic treatments. The substantial reworking of the epigenetic and chromatin landscape that occurs with cellular senescence has been related to such effector pathways. These age-related epigenetic alterations and their influence on senescence phenotypes particularly proliferative arrest and senescence-associated secretory phenotypes are discussed (SASP). Im also looking at epigenetic targets for suppressing the harmful effects of senescent cells which lead to ageing. Senescence is a cellular condition brought on by internal or external stressors that causes cell cycle halt morphological alterations mitochondrial and lysosomal dysfunction and the senescence-associated secretory phenotype.  Terminally developed somatic cells may now be reprogrammed into pluripotent stem cells or another differentiated state using reprogramming technologies. During cellular reprogramming epigenetic regulation undergoes a dynamic rearrangement. Reprogramming can be used to actively adjust epigenetic regulation since it does not need modifications to the underlying DNA. Although reprogramming has primarily been studied at the cellular level in vitro investigations have shown that somatic cells in multicellular animals may be reprogrammed in vivo.