Long-lived alpha MUPA transgenic mice exhibit increased mitochondrion-mediated apoptotic capacity

Annals of the New York Academy of Sciences
Oren TiroshR Miskin

Abstract

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 alpha MUPA 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 alpha MUPA liver were noted, at the mitochondrial and cellular level, which consistently pointed to an enhanced capacity to induce apoptosis. In addition, alpha MUPA 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 alpha MUPA 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.

References

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Citations

Nov 13, 2007·Aging Cell·Srinivas AyyadevaraRobert J Shmookler Reis
Dec 20, 2017·Oncotarget·Hua-Hua ZhongShu-Long Yang
Jun 15, 2019·Cellular and Molecular Life Sciences : CMLS·Venkat Raghavan KrishnaswamyIrit Sagi
May 26, 2009·Biochimica Et Biophysica Acta·Robert J Shmookler ReisSrinivas Ayyadevara

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis