My work centres on the mechanisms and consequences of cellular senescence. Senescent cells are the living, but permanently non-dividing, forms of cells which are normally capable of division within mammalian tissues. Thus it is possible to have both growing and senescent forms of fibroblasts, keratinocytes, astrocytes, endothelial cells, vascular smooth muscle cells but not neurons or red blood cells. The senescent state is distinct from quiescence (transient growth arrest induced by contact inhibition or serum withdrawal), from cell death (senescent cells remain viable for many years) and from terminal differentiation. In vivo senescence primarily exists to limit the capacity for expansion of clones of cells and thus limit the opportunities for them to accumulate pro-carcinogenic mutations. When senescence was first observed in vitro in the early 1960s Leonard Hayflick proposed that the phenomenon was related to ageing. Although this theory was bitterly contested for decades it is now clear that the progressive accumulation of senescent cells is a major cause of ageing in mammals. I study three distinct aspects of this process.