Abstract
Cellular senescence is a process by which primary cells detect a stress signal, stop replicating and modify their surrounding microenvironment1,2. The accumulation of senescent cells contributes to organismal ageing3, but the precise mechanisms regulating this process are not well understood. Our lab has recently described the need for the interaction of focal adhesion (FA) with the extracellular matrix (ECM) regulating senescence and ageing, by activating the TGFb pathway4. However, the mechanisms implicated, the impact throughout ageing and the discovery of therapeutic targets to tackle senescent cells regulating FA, have not been addressed.
References
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