Effects of cellular senescence on metabolic pathways in non-immune and immune cells.

Many cellular stresses induce cellular senescence and the irreversible arrest of cell proliferation in different cell types. Although blocked in their capacity to divide, senescent cells are metabolically active and are characterized by a different metabolic phenotype as compared to non-senescent cells. Changes observed in senescent cells depend from the cell type and lead to an adaptative flexibility in the type of metabolism.

Lack of consensus on an aging biology paradigm? A global survey reveals an agreement to disagree, and the need for an interdisciplinary framework.

At a recent symposium on aging biology, a debate was held as to whether or not we know what biological aging is. Most of the participants were struck not only by the lack of consensus on this core question, but also on many basic tenets of the field. Accordingly, we undertook a systematic survey of our 71 participants on key questions that were raised during the debate and symposium, eliciting 37 responses.

Mitochondrial Lon protease - depleted HeLa cells exhibit proteome modifications related to protein quality control, stress response and energy metabolism.

The ATP-dependent Lon protease is located in the mitochondrial matrix and oxidized proteins are among its primary targets for their degradation. Impairment of mitochondrial morphology and function together with apoptosis were observed in lung fibroblasts depleted for Lon expression while accumulation of carbonylated mitochondrial proteins has been reported for yeast and HeLa Lon deficient cells. In addition, age-related mitochondrial dysfunction has been associated with an impairment of Lon expression.