Crosstalk of clock gene expression and autophagy in aging.

Autophagy and the circadian clock counteract tissue degeneration and support longevity in many organisms. Accumulating evidence indicates that aging compromises both the circadian clock and autophagy but the mechanisms involved are unknown. Here we show that the expression levels of transcriptional repressor components of the circadian oscillator, most prominently the human Period homologue , are strongly reduced in primary dermal fibroblasts from aged humans, while raising the expression of in the same cells partially restores diminished autophagy levels.