Abstract
Rapidly expanding aging populations and a concomitant increase in the prevalence of age-related diseases are global health problems today. Over the past three decades, a large body of work has led to the identification of genes and regulatory networks that affect longevity and health span, often benefiting from the tremendous power of genetics in vertebrate and invertebrate model organisms. Interestingly, many of these factors appear linked to lipids, important molecules that participate in cellular signaling, energy metabolism, and structural compartmentalization. Despite the putative link between lipids and longevity, the role of lipids in aging remains poorly understood. Emerging data from the model organism Caenorhabditis elegans suggest that lipid composition may change during aging, as several pathways that influence aging also regulate lipid metabolism enzymes; moreover, some of these enzymes apparently play key roles in the pathways that affect the rate of aging. By understanding how lipid biology is regulated during C. elegans aging, and how it impacts molecular, cellular, and organismal function, we may gain insight into novel ways to delay aging using genetic or pharmacological interventions. In the present review we discuss recent insights into the roles of lipids in C. elegans aging, including regulatory roles played by lipids themselves, the regulation of lipid metabolic enzymes, and the roles of lipid metabolism genes in the pathways that affect aging.
Highlights
One of the most desirable goals in biomedical research is to understand the molecular mechanisms that promote healthy aging
Emerging data from the model organism Caenorhabditis elegans suggest that lipid composition may change during aging, as several pathways that influence aging regulate lipid metabolism enzymes; some of these enzymes apparently play key roles in the pathways that affect the rate of aging
Depletion of the prohibitins extends life span in several genetic backgrounds, including insulin-like growth factor (IGF) signaling (IIS) pathway mutants, mitochondrial mutants, and the eat-2 mutants mimicking dietary restriction; in contrast, reduced prohibitin levels shorten the lifespan in wild-type animals, suggesting that prohibitins act in a context-specific fashion
Summary
One of the most desirable goals in biomedical research is to understand the molecular mechanisms that promote healthy aging. Several genetic and nutritional conditions have been identified that extend mean and/or maximal life span and postpone the onset of phenotypes associated with aging, such as a loss of mobility, a decline in cognitive ability, and others. It has been almost 30 years since single gene mutations were first found to affect aging in the nematode Caenorhabditis elegans (reviewed in Kenyon, 2010a).
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