Many methods of extending life by slowing aging in laboratory animals depend upon increased autophagy, the processes of cellular maintenance that clear out damaged components and proteins. Calorie restriction is one of these methods, for example: some studies have shown that if autophagy is disabled then calorie restriction no longer extends life to a significant degree.
[Scientists] have identified a key factor that regulates the autophagy process, a kind of cleansing mechanism for cells in which waste material and cellular debris is gobbled up to protect cells from damage, and in turn, modulates aging. [The researchers] found a transcription factor - an on/off switch for genes - that induces autophagy in animal models, including the nematode C. elegans. [This] transcription factor, called HLH-30, coordinates the autophagy process by regulating genes with functions in different steps of the process. Two years ago, researchers discovered a similar transcription factor, or orthologue, called TFEB that regulates autophagy in mammalian cells.
"HLH-30 is critical to ensure longevity in all of the long-lived C. elegans strains we tested. These models require active HLH-30 to extend lifespan, possibly by inducing autophagy. We found this activation not only in worm longevity models, but also in dietary-restricted mice, and we propose the mechanism might be conserved in higher organisms as well."
HLH-30 is the first transcription factor reported to function in all known autophagy-dependent longevity paradigms, strengthening the emerging concept that autophagy can contribute to long lifespan. In a previous study, [researchers] discovered that increased autophagy has an anti-aging effect, possibly by promoting the activity of an autophagy-related, fat-digesting enzyme. With these findings, scientists now know a key component of the regulation of autophagy in aging. Autophagy has become the subject of intense scientific scrutiny over the past few years, particularly since the process - or its malfunction - has been implicated in many human diseases, including cancer, Alzheimer's, as well as cardiovascular disease and neurodegenerative disorders. HLH-30 and TFEB may represent attractive targets for the development of new therapeutic agents against such diseases.