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
**Postponed**
Please save the new dates:
December 12-15, 2021
click HERE for past conferences
More senescence conferences...
Cell Senescence News
Members Featured Articles
The Jekyll and Hyde of Senescence in Cancer: TIMP1 Controls the Switch from Tumor-Controlling to Tumor-Promoting Senescence
Sabela Da Silva-Álvarez, Manuel Collado
Cellular senescence is a response with two faces in cancer: it restricts tumor proliferation, but it can also promote cancer progression and metastasis. In this issue of Cancer Cell, Guccini et al. uncover the role of TIMP1 in prostate cancer allowing a switch from tumor-controlling to tumor-promoting senescence.
Refers to:
Senescence Reprogramming by TIMP1 Deficiency Promotes Prostate Cancer Metastasis
Cancer Cell, Volume 39, Issue 1, 11 January 2021, Pages 68-82.e9
More ICSA members featured articles here
Paper of the Month
NAD+boosting reduces age-associated amyloidosis and restores mitochondrial homeostasis in muscle
Mario Romani, Vincenzo Sorrentino, Chang-Myung Oh, Hao Li, Tanes Imamura de Lima, Hongbo Zhang, Minho Shong, and Johan Auwerx
Aging is characterized by loss of proteostasis and mitochondrial homeostasis. Here, we provide bio-informatic evidence of dysregulation of mitochondrial and proteostasis pathways in muscle aging anddiseases. Moreover, we show accumulation of amyloid-like deposits and mitochondrial dysfunction duringnatural aging in the body wall muscle ofC.elegans, in human primary myotubes, and in mouse skeletal mus-cle, partially phenocopying inclusion body myositis (IBM). Importantly, NAD+homeostasis is critical tocontrol age-associated muscle amyloidosis. Treatment of either aged N2 worms, a nematode model of am-yloid-beta muscle proteotoxicity, human aged myotubes, or old mice with the NAD+boosters nicotinamideriboside (NR) and olaparib (AZD) increases mitochondrial function and muscle homeostasis while attenuatingamyloid accumulation. Hence, our data reveal that age-related amyloidosis is a contributing factor to mito-chondrial dysfunction and that both are features of the aging muscle that can be ameliorated by NAD+meta-bolism-enhancing approaches, warranting further clinical studies.
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
Andrea Maier
Royal Melbourne Hospital
University of Melbourne,
Australia
Gerardo Ferbeyre
Département de biochimie
Faculté de Médecine
Université de Montréal
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