Cellular senescence is a state of irreversible cell cycle arrest that can be triggered by a variety of stress signals. Some examples of these stressors include telomeric shortening, mitochondrial dysfunction, oncogene activation, DNA damage, chromatin disorganization, oxidative stress, and inflammation.

Senescence is marked by an increase in lysosomal activity, complex changes in gene expression, cell structural reorganization, metabolic activity, and the development of a senescence-associated secretory phenotype (SASP). The SASP is typified by the secretion of a diverse arsenal of immunomodulatory, metabolic, and growth regulatory factors, as well as extracellular matrix components and regulators. The scope and complexity of SASPs vary widely depending on the cell type and environment, and the type of cellular senescence. Multiple interconnected signaling networks promote the SASP through transcriptional and translational control of SASP factor production.

Senescent cells stop dividing but remain viable and are resistant to apoptosis, thus accumulating over time. Additionally, as senescent programs are fueled by triggers that are known to increase with age, cellular senescence has been strongly implicated in human aging, cancer progression, and other age-related diseases. Senotherapeutic drugs that specifically target and regulate senescent cells have been developed to help understand the molecular mechanisms that contribute to aging and to potentially combat age-related diseases and dysfunctions.

Curators used information from published literature, Reactome, and Gene Ontology to develop a list of genes known to be part of cellular senescence pathways. The genes have been annotated into sub categories of cell cycle arrest (factors that induce senescence or are involved in the signaling pathways that result in senescent cell cycle arrest), SASP signaling, and SASP factors.

The Cell Cycle - Senescence curation project is on-going and will be updated each month. If you notice errors or missing interactions/publications in this dataset, or otherwise wish to contribute to this project, please contact us at support@thebiogrid.org. All Cell Cycle - Senescence database records are freely available for download from links within this project.