concept

senescence-associated secretory phenotype

Also known as: senescent secretory phenotype, SASP, cellular senescence-associated secretory phenotype, senescence-associated secretory phenotypes, inflammatory senescence-associated secretory phenotype

Facts (34)

Sources

Cellular rejuvenation: molecular mechanisms and potential ... - Nature nature.com Nature Mar 14, 2023 22 facts

claimSenolytics, which remove senescent cells, and senomorphics, which attenuate the senescence-associated secretory phenotype (SASP), can ameliorate diabetes and its complications by alleviating insulin resistance and reducing tissue inflammation.

claimCartilage deterioration is linked to the Senescence-Associated Secretory Phenotype (SASP), while age-related mitochondrial dysfunction and oxidative stress may cause senescence in joint tissue cells.

claimOsteoarthritis (OA) is a degenerative disease of the cartilage that develops with aging and shares a pathogenesis with the Senescence-Associated Secretory Phenotype (SASP) and senescence of joint tissue cells.

claimSenomorphics can be achieved through the use of specific neutralizing antibodies against individual SASP factors.

claimJAK inhibitors repress SASP function, alleviate systemic inflammation, and enhance physical function.

claimSASP inhibitors require continuous treatment to maintain suppression of the Senescence-Associated Secretory Phenotype (SASP), which increases the likelihood of side effects compared to the intermittent administration of senolytic drugs.

claimSenescent skin cells, senescence-associated secretory phenotype (SASP), oxidative stress, inflammation, and autophagy mediate the pathophysiology of skin ageing.

claimSenolytics, which kill senescent cells and stop the bystander effects of the senescence-associated secretory phenotype (SASP), are a potential treatment for age-related macular degeneration (AMD) due to the role of cellular senescence in its pathogenesis.

claimSenomorphics, also known as SASP inhibitors, target pathways such as p38 MAPK, JAK/STAT, and interleukins to attenuate the senescence-associated secretory phenotype (SASP) of senescent cells.

claimSenescent cell (SC) elimination and senescence-associated secretory phenotype (SASP) inhibition have demonstrated efficacy in clinical studies for treating functional degeneration and chronic diseases associated with ageing.

claimROCK inhibition modulates the senescence-associated secretory phenotype (SASP) in oral keratinocytes, as reported in a 2020 study in FEBS Open Bio.

claimCellular senescence, stress-induced premature ageing, the senescence-associated secretory phenotype (SASP), oxidative stress, and inflammation contribute to the development of chronic kidney disease (CKD).

claimThe senescence-associated secretory phenotype (SASP) has potential as a therapeutic target for senescence-associated diseases.

claimDrugs targeting senescence-associated secretory phenotype (SASP), such as glucocorticoids, resveratrol, and protease inhibitors, attenuate chronic kidney disease (CKD) primarily by inhibiting NF-κB signals and reducing reactive oxygen species (ROS).

claimSmall molecule inhibitors of p38 MAP kinase and MK2 can suppress the senescence-associated secretory phenotype (SASP) in human fibroblasts, as demonstrated in a 2016 study in Biogerontology.

claimAnti-PD-1/PD-L1 administration ameliorates age-associated functional decline in vivo, including decreased senescence-associated secretory phenotypes (SASPs) and inflammation, while improving alveolar volume, liver fat accumulation, grip strength, and athletic ability.

claimSenescence-associated secretory phenotype (SASP) can contribute to angiogenesis, facilitate tumor development, induce epithelial-mesenchymal transition (EMT) in neighboring cancer cells, and induce extracellular matrix (ECM) degradation, which results in the migration and metastasis of cancer cells.

claimThe p38MAPK inhibitors SB203580, UR-13756, and BIRB 796 potently suppress SASP expression in senescent cells.

claimClearance of senescent cells (SCs) and decreasing the senescence-associated secretory phenotype (SASP) benefit organ repair and disease treatment, but senolytics often have poor cell selectivity that may damage normal tissue, and SASP inhibitors targeting specific secretory factors have limited therapeutic effects on multiple factors-mediated diseases.

claimApigenin suppresses the senescence-associated secretory phenotype and its paracrine effects on breast cancer cells, according to a 2017 study in Geroscience.

claimGlucocorticoids suppress selected components of the senescence-associated secretory phenotype, as reported in a 2012 study in Aging Cell.

claimIn chronic wounds, the interaction between senescent cells and the extracellular matrix is a barrier to healing because senescent cells produce Senescence-Associated Secretory Phenotype (SASP) factors and Reactive Oxygen Species (ROS), which increase matrix proteolysis, cause inflammation, impair vascular endothelial cells, and create a microenvironment that accelerates further cellular senescence.

Cellular senescence: from homeostasis to pathological implications ... frontiersin.org Frontiers 6 facts

claimThe senescence-associated secretory phenotype is a regulated biological process.

referenceThe article "Recent advances in senescence-associated secretory phenotype and osteoporosis" was published in the journal Heliyon in 2024 (Volume 10, article e25538).

claimEZH2 inhibition remodels the inflammatory senescence-associated secretory phenotype to potentiate pancreatic cancer immune surveillance.

claimThe mTOR pathway regulates the pro-tumorigenic senescence-associated secretory phenotype by promoting the translation of IL1A.

claimThe protein hnRNP A1 antagonizes cellular senescence and the senescence-associated secretory phenotype by regulating the stability of SIRT1 mRNA.

referenceLiu P, Liu F, Lin J, Fukumoto T, Nacarelli T, Hao X et al. reported in Nature Cell Biology (2021) that m6A-independent genome-wide redistribution of METTL3 and METTL14 drives the senescence-associated secretory phenotype.

Chronic inflammation in the etiology of disease across the life span nature.com Nature Dec 5, 2019 3 facts

claimPartial sleep deprivation activates the DNA damage response (DDR) and the senescence-associated secretory phenotype (SASP) in aged adult humans, as reported in a 2016 study in Brain, Behavior, and Immunity.

claimCellular senescence and the senescent secretory phenotype are linked to age-related chronic diseases, according to a 2014 review in Current Opinion in Clinical Nutrition and Metabolic Care.

claimLong-term exposure to persistent organic pollutants induces telomere dysfunction and the senescence-associated secretory phenotype, according to a 2018 study in The Journals of Gerontology: Series A.

Inflammation: a matter of immune cell life and death - Nature nature.com Nature Mar 4, 2025 1 fact

referenceWang, B., Han, J., Elisseeff, J. H. & Demaria, M. (2024) reviewed the senescence-associated secretory phenotype and its physiological and pathological implications, published in Nat. Rev. Mol. Cell Biol. 1–21.

Targeting immunosenescence and inflammaging - Nature nature.com Nature Sep 1, 2025 1 fact

claimJAK inhibition alleviates the cellular senescence-associated secretory phenotype (SASP) and frailty in old age.

Role of Inflammation in Tissue Regeneration and Repair - OUCI ouci.dntb.gov.ua Sheetal Saini, Prankrishna Kakati, Kulwant Singh · Springer Nature Singapore 1 fact

referenceThe senescence-associated secretory phenotype (SASP) is described as the 'dark side of tumor suppression' in a 2010 review by Coppe, Desprez, Krtolica, and Campisi published in the Annual Review of Pathology.