Anti-inflammatory drugs extend longevity in animal models with accelerated aging
October 02, 2012
The prestigious journal Genes & Depelopment publishes a study carried out by a research team at the University of Oviedo
An article published this week by the prestigious journal Genes & Development by scientists at the Institutes of Oncology and Odontology of the University of Oviedo has revealed the importance of the inflammation in the development of accelerated aging symptoms casued by nuclear envelope defects.
The accelerated aging symptoms are diseases characterised by the premature signs of several alterations related to normal aging. This work, led by Carlos López-Otín and José María Pérez Freije, goes in depth in the study of the mechanisms responsible for the develpment of these symptoms by the use of murine models, which recap the main characteristics of the Hutchinson-Gilford Progeria Syndrome, a desease caused by the accumulation of abnormal forms of prelamin A in the nuclear envelope.
For doing this job, the researchers have developed a new method for the analysis in vivoof the biochemical route of NF-κB, the main cellular anti-inflammatory mediator, demonstrating at the same time that progeroyd mice show greater activation in this route as well as an increase of pro-inflamatory molecules in blood. In order to explain the accidental relation between the activation of NF-κB and accelerated aging, the authors made use of two complementary approaches aimed at reducing the activation of this inflammatory route. Thus, both the use of a genetic approach and the administration of anti-inflammatory substances were able to prevent the activation of the NF-kB route reverting serious alterations in the skin and immune system to their usual form and extending the life in the mice treated up to a 30%.
All together, the results obtained underline the importance of the inflammatory routes in the development of aging. Furthermore, they guarantee the use of anti-inflammatory drugs for the treatment of accelerated aging symptoms as well as for interceding in some of the alterations associated with normal aging.
Reference: Osorio FG, Bárcena C, Soria-Valles C, Ramsay AJ, de Carlos F, Cobo J, Fueyo A, Freije JM, and López-Otín C. "Nuclear lamina defects cause ATM-dependent NF-κB activation and link accelerated aging to a systemic inflammatory response" Genes Dev. 2012