Accelerated ageing in mice deficient in Zmpste24 protease is linked to p53 signalling activation

Ignacio Varela, Juan Cadiñanos, Alberto M. Pendás, Ana Gutiérrez-Fernández, Alicia R. Folgueras, Luis M. Sánchez, Zhongjun Zhou, Francisco J. Rodríguez, Colin L. Stewart, José A Vega, Karl Tryggvason, José M. P. Freije and Carlos López-Otín ()
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Ignacio Varela: Instituto Universitario de Oncología
Juan Cadiñanos: Instituto Universitario de Oncología
Alberto M. Pendás: Instituto Universitario de Oncología
Ana Gutiérrez-Fernández: Instituto Universitario de Oncología
Alicia R. Folgueras: Instituto Universitario de Oncología
Luis M. Sánchez: Instituto Universitario de Oncología
Zhongjun Zhou: Karolinska Institutet
Francisco J. Rodríguez: Instituto Universitario de Oncología
Colin L. Stewart: National Cancer Institute
José A Vega: Universidad de Oviedo
Karl Tryggvason: Karolinska Institutet
José M. P. Freije: Instituto Universitario de Oncología
Carlos López-Otín: Instituto Universitario de Oncología

Nature, 2005, vol. 437, issue 7058, 564-568

Abstract: Linking p53 and ageing A paper published in Nature in January 2002 caught the attention of those working on both ageing and cancer researcher: mice with a hyperactive p53 tumour suppressor gene were resistant to cancer but, here was the surprise, also showed signs of premature ageing. The link between p53 signalling and ageing is further explored in a study of the molecular mechanisms behind the striking accelerated ageing observed in mutant mice deficient in a metalloprotease called Zmpste24, a condition similar to some premature ageing syndromes in humans. The protease deficiency induces a p53 signalling pathway, accompanied by increased cellular senescence and accelerated ageing at the organismal level.

Date: 2005
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DOI: 10.1038/nature04019

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