Cellular senescence is generally an irreversible proliferative arrest in damaged normal cells that have exited the cell cycle. These cells display high metabolic activities [1], remain viable, and actively suppress apoptosis [2, 3]. Senescent cells present unique morphological and molecular characteristics and functions that distinguish them from other nondividing cell populations, such as quiescent cells and terminally differentiated cells [4, 5, 6]. The hallmarks of cellular senescence include: prolonged cell cycle arrest, transcriptional changes, acquisition of a bioactive secretome, known as the senescence-associated secretory phenotype (SASP), macromolecular damage, and deregulated metabolism [7].

Replicative senescence was the first cellular senescence subtype to be described [8]. It is induced after serial propagation of normal human cells in culture and is caused by telomere erosion and the consequent increase in DNA lesions [9, 10,11,12]. The limited lifespan of most (perhaps all) cultured primary cells is influenced by the species and tissue type from which they were derived. Senescence can also be triggered by many other intrinsic and extrinsic factors, particularly, replicative stress, oxidative damage, metabolism dysfunctions, cytokines, oncogene activation, and chemotherapy agents. All these factors can induce DNA damage and senescence in normal and cancer cells (in some contexts) [6]. Cellular senescence occurs not only in vitro (i.e., cell culture models), but also in various tissues in vivo [13,14,15,16].

Senescence is an important contributor to cancer and aging, two processes characterized by a time-dependent accumulation of cell damage and dysfunction. Senescence markers are detected in premalignant tumor lesions but not at later stages of tumor development [17,18,19]. The proliferative arrest imposed by cellular senescence represents an early barrier against cancer initiation by preventing the propagation of damaged DNA to the next generation of cells [18,20]. Therefore, it has been proposed that senescence escape is required for tumor progression to overt malignancy [18,21]. On the other hand, senescent fibroblasts can influence their local environment by turning into proinflammatory cells that can promote the growth of transformed or preneoplastic neighboring epithelial cells in culture and in vivo [22,23,24].

A UCLA study in mice reveals that aging muscle stem cells accumulate a protein that slows repair but boosts survival. This protein, NDRG1, acts like a brake, preventing cells from activating quickly after injury. When researchers blocked it in older mice, muscle healing sped up dramatically — but stem cells became less resilient over time. The work suggests aging may reflect a survival trade-off rather than straightforward decline.

A new study describes a technique that rejuvenates aging blood-forming stem cells and could help reduce the risk of age-related blood disorders.