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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

 

ICSA2022

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**ICSA2022 Groningen has been scheduled**

29th of September to 1st of October 2022

More details soon!

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click HERE for past conferences

More senescence conferences...

 

Cell Senescence News

 
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Members Featured Articles

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Dynamic regulation of myofibroblast phenotype in cellular senescence

Irene López-Antona, Constanza Contreras-Jurado, Laura Luque-Martín, Antonio Carpintero-Leyva, Paula González-Méndez, Ignacio Palmero

Cellular senescence is an antiproliferative response with a critical role in the control of cellular balance in diverse physiological and pathological settings. Here, we set to study the impact of senescence on the regulation of cell plasticity, focusing on the regulation of the myofibroblastic phenotype in primary fibroblasts. Myofibroblasts are contractile, highly fibrogenic cells with key roles in wound healing and fibrosis. Using cellular models of fibroblast senescence, we find a consistent loss of myofibroblastic markers and functional features upon senescence implementation. This phenotype can be transmitted in a paracrine manner, most likely through soluble secreted factors. A dynamic transcriptomic analysis during paracrine senescence confirmed the non-cell-autonomous transmission of this phenotype. Moreover, gene expression data combined with pharmacological and genetic manipulations of the major SASP signaling pathways suggest that the changes in myofibroblast phenotype are mainly mediated by the Notch/TGF-β axis, involving a dynamic switch in the TGF-β pathway. Our results reveal a novel link between senescence and myofibroblastic differentiation with potential implications in the physiological and pathological functions of myofibroblasts.

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More ICSA members featured articles here

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Paper of the Month

TRPC3 shapes the ER-mitochondria Ca 2+ transfer characterizing tumour-promoting senescence

 

Valerio Farfariello, Dmitri V. Gordienko, Lina Mesilmany, Yasmine Touil, Emmanuelle Germain, Ingrid Fliniaux, Emilie Desruelles, Dimitra Gkika, Morad Roudbaraki, George Shapovalov, Lucile Noyer, Mathilde Lebas, Laurent Allart, Nathalie Zienthal-Gelus, Oksana Iamshanova, Franck Bonardi, Martin Figeac, William Laine, Jerome Kluza, Philippe Marchetti, Bruno Quesnel, Daniel Metzger, David Bernard, Jan B. Parys, Loïc Lemonnier & Natalia Prevarskaya

Cellular senescence is implicated in a great number of diseases including cancer. Although alterations in mitochondrial metabolism were reported as senescence drivers, the underlying mechanisms remain elusive. We report the mechanism altering mitochondrial function and OXPHOS in stress-induced senescent fibroblasts. We demonstrate that TRPC3 protein, acting as a controller of mitochondrial Ca2+ load via negative regulation of IP3 receptor-mediated Ca2+ release, is down regulated in senescence regardless of the type of senescence inducer. This remodelling promotes cytosolic/mitochondrial Ca2+ oscillations and elevates mitochondrial Ca2+ load, mitochondrial oxygen consumption rate and oxidative phosphorylation. Re-expression of TRPC3 in senescent cells diminishes mitochondrial Ca2+ load and promotes escape from OIS-induced senescence. Cellular senescence evoked by TRPC3 downregulation in stromal cells displays a proinflammatory and tumour-promoting secretome that encourages cancer epithelial cell proliferation and tumour growth in vivo. Altogether, our results unravel the mechanism contributing to pro-tumour behaviour of senescent cells.

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

 

About ICSA

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Treasurer

Sushma-Nagaraja Grellscheid, 

Durham University,

Durham, UK

University of Bergen, Norway

President
Marco Demaria
Faculty of Medical Sciences
University of Groningen,
Netherlands

Vice President

Lars Zender

University Hospital Tübingen,

Tübingen, Germany

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Secretary

Romuald Binet,

 Ludwig Institute for Cancer Research, Oxford, UK

Steering Committee Members

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Peter Adams

Sanford Burnham Prebys Medical Discovery Institute, La Jolla

California, USA

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Cleo Bishop
Senior Lecturer
Blizard Institute

London, UK
 

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Masashi Narita

CRUK Cambridge Institute

University of Cambridge

Cambridge, UK

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Judith Campisi

Buck Institute for Research on Aging
Lawrence Berkeley National Laboratory

California, USA

Manuel Collado,
Health Research Institute of Santiago de Compostela,

Santiago de Compostela, Spain

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Manuel Serrano

Institute for Research

and Biomedicine, Barcelona, 

Spain

 

Daniel Muñoz-Espin

Cambridge Biomedical Campus

University of Cambridge

Cambridge, UK

Eiji Hara

Osaka University

Osaka, Japan

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Andrea Maier

Centre for Healthy Longevity, National University of Singapore, Singapore

Sheila A. Stewart

ICCE Institute

Washington University School of Medicine, St. Louis, USA

 

Learn More

 

ICSA Membership

How to join ICSA?

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

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  • Student/Postdoc - 25€

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