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

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ICSA2020 #icsa2020osaka

http://www.icsa2020-osaka.jp

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

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

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Paper of the Month

Reprogramming to recover youthful epigenetic information and restore vision

Yuancheng Lu, Benedikt Brommer, Xiao Tian, Anitha Krishnan, Margarita Meer, Chen Wang, Daniel L. Vera, Qiurui Zeng, Doudou Yu, Michael S. Bonkowski, Jae-Hyun Yang, Songlin Zhou, Emma M. Hoffmann, Margarete M. Karg, Michael B. Schultz, Alice E. Kane, Noah Davidsohn, Ekaterina Korobkina, Karolina Chwalek, Luis A. Rajman, George M. Church, Konrad Hochedlinger, Vadim N. Gladyshev, Steve Horvath, Morgan E. Levine, Meredith S. Gregory-Ksander, Bruce R. Ksander, Zhigang He & David A. Sinclair

Ageing is a degenerative process that leads to tissue dysfunction and death. A proposed cause of ageing is the accumulation of epigenetic noise that disrupts gene expression patterns, leading to decreases in tissue function and regenerative capacity. Changes to DNA methylation patterns over time form the basis of ageing clocks4, but whether older individuals retain the information needed to restore these patterns—and, if so, whether this could improve tissue function—is not known. Over time, the central nervous system (CNS) loses function and regenerative capacity. Using the eye as a model CNS tissue, here we show that ectopic expression of Oct4 (also known as Pou5f1), Sox2 and Klf4 genes (OSK) in mouse retinal ganglion cells restores youthful DNA methylation patterns and transcriptomes, promotes axon regeneration after injury, and reverses vision loss in a mouse model of glaucoma and in aged mice. The beneficial effects of OSK-induced reprogramming in axon regeneration and vision require the DNA demethylases TET1 and TET2. These data indicate that mammalian tissues retain a record of youthful epigenetic information—encoded in part by DNA methylation—that can be accessed to improve tissue function and promote regeneration in vivo.