Role of subcytotoxic stress in tissue ageing

Abstract

Most commonly stress-induced premature senescence (SIPS) is defined as the long-term effects of subcytotoxic stress on proliferative cell types, including appearance of features of replicative senescence. An integrative model of signal transduction can explain the occurrence of SIPS. Cells in SIPS display differences at the level of protein expression which are either common with replicative senescence, or are specific ‘molecular scars’ of the stress. These proteins with changes of expression level affect energy metabolism, defence systems, redox potential, cell morphology and transduction pathways. In vivo, cells capable of proliferation are often exposed to various stresses which nature depends on their location in the body, or on particular conditions such a local asymptomatic microinflammation. Several studies already showed the occurrence of prematurely senescent cells in vivo. Lastly, human ageing is characterised by an increase in proinflammatory cytokines, favouring the installation of a pro-inflammatory state and most likely SIPS.