Replicative senescence is a state that cells enter after a certain number of divisions, also known as the Hayflick limit, which is typically around 40-60 divisions for human cells. The concept is named after Leonard Hayflick, who discovered this phenomenon in the 1960s.

When cells reach this limit, they enter a state of growth arrest known as replicative senescence. They are still alive and metabolically active, but they no longer divide. This state is thought to be a defense mechanism against the development of cancer, as it prevents cells with damaged DNA from dividing uncontrollably.

A key mechanism behind replicative senescence is telomere shortening. Telomeres are the protective caps on the ends of chromosomes, and they shorten each time a cell divides. Telomerase, an enzyme that replenishes telomeres, is not active in most adult somatic cells. Thus, with each division, the telomeres get progressively shorter. When they become too short, the cell can detect this as DNA damage and trigger senescence to prevent further division.

Besides telomere shortening, other stressors can also induce a similar senescent state, such as DNA damage, oxidative stress, and oncogene activation. This is often referred to as stress-induced premature senescence (SIPS).

Senescent cells contribute to aging and age-related diseases. They secrete pro-inflammatory and tissue-remodeling molecules, a phenomenon known as the senescence-associated secretory phenotype (SASP), which can promote tissue aging and chronic inflammation. Therefore, targeting senescent cells for removal or modulating the SASP are active areas of research in the field of aging biology.