Cell-Nonautonomous Mechanisms Underlying Cellular and Organismal Aging

Six plant extracts delay yeast chronological aging through different signaling pathways

“…Among such diseases are arthritis, diabetes, heart disease, kidney disease, liver dysfunction, sarcopenia, stroke, neurodegenerative diseases (including Parkinson's, Alzheimer's and Huntington's diseases), and many forms of cancer [3, 6, 9, 12, 15–18, 21, 79, 94–105]. Because the major aspects of aging and age-related pathology are conserved across phyla [1, 4–6, 10–13, 16–18], it is noteworthy that this study, recent findings [78] and our ongoing research have revealed several features of the six PEs as potential interventions for decelerating chronic diseases of old age. These features are the following: 1) the six PEs are caloric restriction (CR) mimetics that imitate the aging-delaying effects of the CR diet in yeast under non-CR conditions; 2) they are geroprotectors that slow yeast aging by eliciting a hormetic stress response; 3) they extend yeast longevity more efficiently than any lifespan-prolonging chemical compound yet described; 4) they delay aging through signaling pathways and protein kinases implicated in such age-related pathologies as type 2 diabetes, neurodegenerative diseases, cardiac hypertrophy, cardiovascular disease, sarcopenia and cancers; and 5) they extend longevity and delay the onset of age-related diseases in other eukaryotic model organisms.…”

“…Studies in S. cerevisiae have demonstrated that the major aspects of biological aging are evolutionarily conserved [1, 4–6, 10–13, 16–18]. One of these aspects is the convergence of certain signaling pathways and protein kinases into a network that controls the rate of aging [1, 6, 11, 19–31].…”

Brain–gut communications via distinct neuroendocrine signals bidirectionally regulate longevity in C. elegans

“…This also suggests that IL1 neurons extend life span at lower temperatures by stimulating DAF-16 in the intestine. It is worth noting that, similar to the nervous system, the intestine is also a signaling center that integrates and disseminates longevity signals (Medkour et al 2016).…”

“…As animals and humans get older, all of the tissues/organs age and lose functions, albeit at different rates, resulting in an increased probability of death Sehl et al 2005). Tissue-tissue communications play a key role in choreographing such a body-wide process (Apfeld and Kenyon 1998;Libina et al 2003;Alcedo and Kenyon 2004;Murphy et al 2007;Medkour et al 2016). Work in the past two decades has greatly advanced our understanding of how various genes modulate longevity by regulating the physiology of individual organelles, cells, and tissues (Kenyon 2010;Fontana and Partridge 2015).…”

“…Second, as the brain mediates the interaction between the organism and its surrounding environment by sensing and processing environmental cues, it sits at a key position to integrate environmental signals and internal physiological states to modulate longevity (Allen et al 2015). Indeed, recent work in model organisms such as Caenorhabditis elegans has pointed to an increasingly important role for the brain in regulating longevity by signaling distal tissues, particularly the gut (Alcedo and Kenyon 2004;Durieux et al 2011;Taylor and Dillin 2013;Burkewitz et al 2015;Leiser et al 2015;Medkour et al 2016). However, how such brain-gut communications shape longevity is not well understood.…”