Sex-specific molecular hallmarks point to increased atherogenesis susceptibility in male senescence-accelerated mice.

Aims: The senescence-accelerated mouse (SAM) model has been extensively used to study neurological alterations associated with aging. The SAM model has also proved to be useful in the study of vascular aging, but there is still work to be done to better define its utility as a model of atherosclerosis, since contradictory data have been published and sex seems to play a crucial role in potential divergences.

Materials And Methods: With this in mind, we aimed to decipher the molecular mechanisms underlying early vascular aging on SAMP8 mice, analyzing the aorta of 10 months-old animals by means of in-depth proteomic analysis, considering sex-specific differences.