International Cell Senescence Association
The association aims to promote research, co-operation and exchange of information among all those interested in any aspect of cellular senescence.
Cellular senescence is a programmed state of stable cell cycle arrest that is accompanied by a complex phenotype. Senescent cells play a role in physiological processes such as tumour suppression, wound healing and embryonic development, whilst paradoxically they can contribute to ageing, cancer and age-related disease.
As such, the field of cellular senescence represents a multidisiplinary research topic.
For review articles on cell senescence click HERE
Please save the new dates:
December 12-15, 2021
click HERE for past conferences
More senescence conferences...
Cell Senescence News
Members Featured Articles
Physiological hypoxia restrains the senescence-associated secretory phenotype via AMPK-mediated mTOR suppression
Cellular senescence is a state of stable proliferative arrest triggered by damaging signals. Senescent cells persist during aging and promote age-related pathologies via the pro-inflammatory senescence-associated secretory phenotype (SASP), whose regulation depends on environmental factors. In vivo, a major environmental variable is oxygenation, which varies among and within tissues. Here, we demonstrate that senescent cells express lower levels of detrimental pro-inflammatory SASP factors in physiologically hypoxic environments, as measured in culture and in tissues. Mechanistically, exposure of senescent cells to low-oxygen conditions leads to AMPK activation and AMPK-mediated suppression of the mTOR-NF-κB signaling loop. Finally, we demonstrate that treatment with hypoxia-mimetic compounds reduces SASP in cells and tissues and improves strength in chemotherapy-treated and aged mice. Our findings highlight the importance of oxygen as a determinant for pro-inflammatory SASP expression and offer a potential new strategy to reduce detrimental paracrine effects of senescent cells..
More ICSA members featured articles here
Paper of the Month
Reprogramming lipid metabolism prevents effector T cell senescence and enhances tumor immunotherapy
Xia Lium, Celine L. Hartman, Lingyun Li, Carolyn J. Albert, Fusheng Si, Aiqin Gao, Lan Huang, Yangjing Zhao, Wenli Lin, Eddy C. Hsueh, Lizong Shen, Qixiang Shao, Daniel F. Hoft, David A. Ford, Guangyong Peng
The functional state of T cells is a key determinant for effective antitumor immunity and immunotherapy. Cellular metabolism, including lipid metabolism, controls T cell differentiation, survival, and effector functions. Here, we report that development of T cell senescence driven by both malignant tumor cells and regulatory T cells is a general feature in cancers. Senescent T cells have active glucose metabolism but exhibit unbalanced lipid metabolism. This unbalanced lipid metabolism results in changes of expression of lipid metabolic enzymes, which, in turn, alters lipid species and accumulation of lipid droplets in T cells. Tumor cells and Treg cells drove elevated expression of group IVA phospholipase A2, which, in turn, was responsible for the altered lipid metabolism and senescence induction observed in T cells. Mitogen-activated protein kinase signaling and signal transducer and activator of transcription signaling coordinately control lipid metabolism and group IVA phospholipase A2 activity in responder T cells during T cell senescence. Inhibition of group IVA phospholipase A2 reprogrammed effector T cell lipid metabolism, prevented T cell senescence in vitro, and enhanced antitumor immunity and immunotherapy efficacy in mouse models of melanoma and breast cancer in vivo. Together, these findings identify mechanistic links between T cell senescence and regulation of lipid metabolism in the tumor microenvironment and provide a new target for tumor immunotherapy.
To learn more about young ICSA (yICSA), click here!
Institute for Research
and Biomedicine, Barcelona,
Ludwig Institute for Cancer Research, Oxford, UK
Steering Committee Members
University Hospital Tübingen,
Health Research Institute of Santiago de Compostela,
Santiago de Compostela, Spain
Charité-Universitätsmedizin Berlin (CVK), and Max-Delbrück-Center for Molecular Medicine, Berlin, German
University of London,
University of Groningen,
Royal Melbourne Hospital
University of Melbourne,
Département de biochimie
Faculté de Médecine
Université de Montréal
Live Longer, Live Well
Telomeres and Cell Senescence
Researchers Extend Lifespan by as Much as 35 Percent in Mice