Results 1 to 10 of about 8,456,945 (252)

Unbiased analysis of senescence associated secretory phenotype (SASP) to identify common components following different genotoxic stresses

open access: yesAging, 2016
Senescent cells secrete senescence-associated secretory phenotype (SASP) proteins to carry out several functions, such as sensitizing surrounding cells to senesce; immunomodulation; impairing or fostering cancer growth; and promoting tissue development.
Özcan, Servet   +6 more
openaire   +5 more sources

Senescence and fibrosis in salivary gland aging and disease

open access: yesJournal of Oral Biology and Craniofacial Research
Salivary gland hypofunction is highly prevalent in aged and diseased individuals leading to significant discomfort and morbidity. One factor that contributes to salivary gland hypofunction is cellular aging, or senescence.
Deirdre A. Nelson   +3 more
doaj   +1 more source

GDF15 is associated with hepatocellular senescence and correlates with mortality in patients with alcohol-associated hepatitis

open access: yesJHEP Reports
Background & Aims: Cellular senescence is characterized by the loss of proliferative capacity, cell cycle arrest, and the acquisition of a proinflammatory senescence-associated secretory phenotype (SASP).
Teresa Rubio-Tomás   +19 more
doaj   +1 more source

Senescence-associated secretory phenotype in lung cancer: remodeling the tumor microenvironment for metastasis and immune suppression

open access: yesFrontiers in Oncology
Cellular senescence exerts dual roles in lung cancer pathogenesis: initially suppressing tumorigenesis via p53/p21/p16-mediated cell cycle arrest, but promoting malignancy through the senescence-associated secretory phenotype (SASP).
Chen Chen   +4 more
doaj   +1 more source

Altered Senescence-Associated Secretory Phenotype of Human Osteoblasts from Patients with Osteoporosis Enhances Endothelial Cell Migration and Proliferation In Vitro

open access: yesBiology
Osteoporosis (OP) is a highly prevalent age-associated inflammatory bone disease that remains underdiagnosed and undertreated despite its substantial global burden.
Lisa Oezel   +9 more
doaj   +1 more source

Cycloastragenol attenuates osteoarthritis by restoring chondrocyte senescence via the NRF2/NF-κB signaling axis

open access: yesScientific Reports
Osteoarthritis (OA) involves oxidative stress-induced chondrocyte senescence and extracellular matrix (ECM) dysregulation, yet disease-modifying therapies remain elusive.
Shuhao Zhang   +5 more
doaj   +1 more source

Apoptosis signal-regulating kinase 1 promotes inflammation in senescence and aging

open access: yesCommunications Biology
Cellular senescence is a stress-induced, permanent cell cycle arrest involved in tumor suppression and aging. Senescent cells secrete bioactive molecules such as pro-inflammatory cytokines and chemokines.
Takeru Odawara   +2 more
doaj   +1 more source

CDK4/6 inhibition induces a senescence-associated secretory phenotype via delayed NF-κB activation

open access: yesLife Science Alliance
Extended therapeutic inhibition of CDK4/6 pushes cancer cells into a senescent-like state and can trigger NF-κB activation to induce an inflammatory signature in both liposarcoma and ER+ breast cancer cells.
Joanna Lan-Hing Yeung   +9 more
doaj   +1 more source

Cell enlargement modulated by GATA4 and YAP instructs the senescence-associated secretory phenotype

open access: yesNature Communications
Dynamic changes in cell size are associated with development and pathological conditions, including aging. Although cell enlargement is a prominent morphological feature of cellular senescence, its functional implications are unknown; moreover, how ...
Joae Joung   +12 more
doaj   +1 more source

A phosphorylation switch in the Mediator MED15 controls cellular senescence and cognitive decline

open access: yesCell Discovery
A hallmark of aging is chronic systemic inflammation, which is exacerbated by the hypersecretory aging phenotype known as the senescence-associated secretory phenotype (SASP).
Haozheng Li   +12 more
doaj   +1 more source

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