Results 11 to 20 of about 29,788 (255)

SASP – Physiotherapy beyond 100 years of rehabilitation

open access: yesSouth African Journal of Physiotherapy
No abstract ...
Witness Mudzi
doaj   +3 more sources

Mitochondrial RNA cytosolic leakage drives the SASP

open access: yesNature Communications
Senescent cells secrete proinflammatory factors known as the senescence-associated secretory phenotype (SASP), contributing to tissue dysfunction and aging. Mitochondrial dysfunction is a key feature of senescence, influencing SASP via mitochondrial DNA (
Stella Victorelli   +22 more
doaj   +3 more sources

SASP reflects senescence [PDF]

open access: yesEMBO reports, 2009
Senescence is a permanent state of cell cycle arrest that—unlike quiescence—is unresponsive to growth factors. Originally described in terms of the replicative exhaustion of cultured fibroblasts (Hayflick & Moorhead, 1961), it has since been shown that senescence can occur prematurely upon oncogene induction and other cellular stresses.
Andrew R J, Young, Masashi, Narita
openaire   +2 more sources

“Bone-SASP” in Skeletal Aging

open access: yesCalcified Tissue International, 2023
AbstractSenescence is a complex cell state characterized by stable cell cycle arrest and a unique secretory pattern known as the senescence-associated secretory phenotype (SASP). The SASP factors, which are heterogeneous and tissue specific, normally include chemokines, cytokines, growth factors, adhesion molecules, and lipid components that can lead ...
Fang, Ching-Lien, Liu, Bin, Wan, Mei
openaire   +2 more sources

TORn about SASP regulation [PDF]

open access: yesCell Cycle, 2015
Senescence is a cellular response to stresses such as oncogenic signaling, DNA damage and telomere loss, characterized by a stable growth arrest.
Nicolás, Herranz   +2 more
openaire   +2 more sources

SASP regulation by noncoding RNA [PDF]

open access: yesMechanisms of Ageing and Development, 2017
Noncoding RNAs (ncRNAs), including micro (mi)RNAs, long noncoding (lnc)RNAs, and circular (circ)RNAs, control specific gene expression programs by regulating transcriptional, post-transcriptional, and post-translational processes. Through their broad influence on protein expression and function, ncRNAs have been implicated in virtually all cellular ...
Amaresh C, Panda   +2 more
openaire   +2 more sources

A proteomic atlas of senescence-associated secretomes for aging biomarker development. [PDF]

open access: yes, 2020
The senescence-associated secretory phenotype (SASP) has recently emerged as a driver of and promising therapeutic target for multiple age-related conditions, ranging from neurodegeneration to cancer.
Basisty, Nathan   +11 more
core   +1 more source

SIN3B, the SASP, and pancreatic cancer [PDF]

open access: yesMolecular & Cellular Oncology, 2014
Cellular senescence is classically considered a tumor suppressive mechanism. In addition to having stably exited the cell cycle, senescent cells secrete inflammatory factors. We recently demonstrated that senescence correlates with accelerated cancer progression in a mouse model of pancreatic ductal adenocarcinoma.
Cantor, David J, David, Gregory
openaire   +2 more sources

Senescence and the SASP: many therapeutic avenues [PDF]

open access: yesGenes & Development, 2020
Cellular senescence is a stress response that elicits a permanent cell cycle arrest and triggers profound phenotypic changes such as the production of a bioactive secretome, referred to as the senescence-associated secretory phenotype (SASP). Acute senescence induction protects against cancer and limits fibrosis, but lingering senescent cells drive age-
Birch, J, Gil, J
openaire   +4 more sources

Defective mitochondria ignite the SASP [PDF]

open access: yesNature Reviews Molecular Cell Biology, 2020
Defective mitochondria in senescent cells activate a signalling pathway that promotes the senescence-associated secretory phenotype and inflammation.
openaire   +2 more sources

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