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

 

ICSA2020 #icsa2020osaka

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**Postponed**

Please save the new dates:

December 12-15, 2021

click HERE for past conferences

More senescence conferences...

COMPARATIVE BIOLOGY OF AGING

15-19 Jun 2020 Roscoff (France)

***Postponed***

 

Cell Senescence News

 
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Members Featured Articles

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Physiological hypoxia restrains the senescence-associated secretory phenotype via AMPK-mediated mTOR suppression

 

Thijmenvan Vliet, Marta Varela-Eirin, Boshi Wang, Michela Borghesan, Simone M.Brandenburg, Rossana Franzin, Konstantinos Evangelou, Marc Seelen, Vassilis Gorgoulis, Marco Demaria

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..

 

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More ICSA members featured articles here

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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.

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Liu2021

To learn more about young ICSA (yICSA), click here!

 

About ICSA

President

Manuel Serrano, 

Institute for Research

and Biomedicine, Barcelona, 

Spain

Vice-President

Oliver Bischof

Institut Pasteur,

Paris, France

Treasurer

Sushma-Nagaraja Grellscheid, 

Durham University,

Durham, UK

Secretary

Romuald Binet,

 Ludwig Institute for Cancer Research, Oxford, UK

Website Manager

Dominick Burton,

Loughborough

University, UK

Steering Committee Members

Lars Zender

University Hospital Tübingen,

Tübingen, Germany

Manuel Collado,
Health Research Institute of Santiago de Compostela,

Santiago de Compostela, Spain

Cleo Bishop
Senior Lecturer
Blizard Institute

London, UK
 

Clemens Schmitt

Charité-Universitätsmedizin Berlin (CVK), and Max-Delbrück-Center for Molecular Medicine, Berlin, German

Dorothy Bennett 

St George's,

University of London,

UK

Marco Demaria

Faculty of Medical Sciences

University of Groningen,

Netherlands

Andrea Maier

Royal Melbourne Hospital

University of Melbourne,

Australia

Gerardo Ferbeyre 

Département de biochimie
Faculté de Médecine
Université de Montréal

Learn More

Live Longer, Live Well

Telomeres and Cell Senescence

Researchers Extend Lifespan by as Much as 35 Percent in Mice

 
 

ICSA Membership

How to join ICSA?

The cost of registration for one year of ICSA membership is:

  • Standard - 50€

  • Student/Postdoc - 25€

To become a member, follow this link.

*** REGISTER NOW FOR 2021 ***

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