Anti-inflammatory Action of Calorie Restriction Underlies the Retardation of Aging and Age-Related Diseases

Abstract

Calorie restriction (CR) is known to extend lifespan and has anti-oxidative properties that lead to physiological and biological resistance against diseases and stress. This chapter reviews the molecular mechanisms of CR's anti-inflammatory actions during aging. The crux of CR's ability to attenuate age-related chronic inflammation is related to its power to maintain redox status by modulating oxidative stress during aging. Here, for better molecular insights, key transcription factors such as FoxO, Nrf2, and PPARs induced by CR are described for their modulation of the age-related inflammation response. In addition, recent analyses by systems biology on chronic inflammation, age-related pro-inflammatory gene activation, and CR's suppression produced evidence identifing various target genes, target molecules, and their networks. The wide implication of the proinflammatory process under pathophysiological conditions are further detailed in this chapter by including autophagic activity and the activation of the recently recognized inflammasome, a component of key innate immunological defenses and ER stress. This chapter summarizes the evidence that CR suppresses molecular inflammation through the proper maintenance of redox status, NF-kappa B signaling, inflammasome activation, ER stress, and insulin sensitivity, which in turn lead to the intervention of aging processes and age-related diseases.