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

http://www.icsa2020-osaka.jp

Postponed

Please save the new dates:

June 7-10, 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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Featured Article

T cells with dysfunctional mitochondria induce multimorbidity and premature senescence

Gabriela Desdín-Micó, Gonzalo Soto-Heredero, Juan Francisco Aranda, Jorge Oller, Elisa Carrasco, Enrique Gabandé-Rodríguez, Eva Maria Blanco, Arantzazu Alfranca, Lorena Cussó, Manuel Desco, Borja Ibañez, Arancha R. Gortazar, Pablo Fernández-Marcos, Maria N. Navarro, Bruno Hernaez, Antonio Alcamí, Francesc Baixauli,María Mittelbrunn

The effect of immunometabolism on age-associated diseases remains uncertain. In this work, we show that T cells with dysfunctional mitochondria owing to mitochondrial transcription factor A (TFAM) deficiency act as accelerators of senescence. In mice, these cells instigate multiple aging-related features, including metabolic, cognitive, physical, and cardiovascular alterations, which together result in premature death. T cell metabolic failure induces the accumulation of circulating cytokines, which resembles the chronic inflammation that is characteristic of aging (“inflammaging”). This cytokine storm itself acts as a systemic inducer of senescence. Blocking tumor necrosis factor–α signaling or preventing senescence with nicotinamide adenine dinucleotide precursors partially rescues premature aging in mice with Tfam-deficient T cells. Thus, T cells can regulate organismal fitness and life span, which highlights the importance of tight immunometabolic control in both aging and the onset of age-associated diseases.