Long-lived αMUPA transgenic mice exhibit increased mitochondrion-mediated apoptotic capacity

Oren Tirosh, Betty Schwartz, Igor Zusman, George Kossoy, Shlomo Yahav, Ruth Miskin*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


Caloric restriction (CR) is currently the only therapeutic intervention known to attenuate aging in mammals, but the mechanisms underlying this phenomenon are still poorly understood. To study this issue, the transgenic model of αMUPA mice, which previously were reported to spontaneously eat less and live longer compared with their wild-type (WT) control mice, were used. Currently, two transgenic lines that eat less are available, thus implicating the transgenic enzyme, that is, the urokinase-type plasminogen activator (uPA), in causing the reduced appetite. Recently, several changes in the αMUPA liver were noted, at the mitochondrial and cellular level, which consistently pointed to an enhanced capacity to induce apoptosis. In addition, αMUPA mice showed a reduced level of serum IGF-1 and a reduced incidence of spontaneously occurring or carcinogen-induced tumors in several tissues. Overall, the αMUPA model suggests that long-lasting, moderately increased apoptotic capacity, possibly linked in part to modulation of serum IGF-1 and mitochondrial functions, could play a role in the attenuation of aging in calorically restricted mice.

Original languageAmerican English
Pages (from-to)439-442
Number of pages4
JournalAnnals of the New York Academy of Sciences
StatePublished - 2004


  • Aging, apoptosis
  • Caloric restriction
  • Mitochondria
  • uPA plasminogen activator
  • αMUPA transgenic mice


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