Abstract
ABSTRACTAutophagy, as the key nutrient recycling pathway, enables eukaryotic cells to adapt to surging cellular stress during aging and, thereby, delays age-associated deterioration. Autophagic flux declines with age and, in turn, decreases in autophagy contribute to the aging process itself and promote senescence. Here, we outline how autophagy regulates immune aging and discuss autophagy-inducing interventions that target senescent immune cells, which are major drivers of systemic aging. We examine how cutting-edge technologies, such as single-cell omics methods hold the promise to capture the complexity of molecular and cellular phenotypes associated with aging, driving the development of suitable putative biomarkers and clinical bioassays. Finally, we debate the urgency to initiate large-scale human clinical trials. We give special preference to small molecule probes and to dietary interventions that can extend healthy lifespan and are affordable for most of the world's population.
Highlights
By 2050, it is estimated that 2 billion people, i.e. >20% of the total world population, will be over 60 years old
Older adults are prone to age-related conditions but are more susceptible to microbial infections and they exhibit diminished vaccine responses due to decreased immune function (Haynes, 2020; Mueller et al, 2020). In this Perspective, we focus on the systemic deterioration of immune function with age, which is accompanied by inflammaging, a chronic state of innate immune activation causing systemic low-grade inflammation (Furman et al, 2019)
Among others, showed that inhibition of mechanistic target of rapamycin complex 1 (mTORC1) activity by rapamycin results in enhanced generation of memory CD8+ T cells providing long-term immunity, which is key in promoting vaccine efficiency, but whether this occurred via autophagy has not been tested (Araki et al, 2009; Turner et al, 2011)
Summary
By 2050, it is estimated that 2 billion people, i.e. >20% of the total world population, will be over 60 years old (key facts on ageing and health, WHO, 2021). Defects in autophagy are connected to a variety of human illnesses, including immune-associated and age-related diseases, which are both often linked to increased inflammation (Aman et al, 2021; Klionsky et al, 2021). Among others, showed that inhibition of mTORC1 activity by rapamycin results in enhanced generation of memory CD8+ T cells providing long-term immunity, which is key in promoting vaccine efficiency, but whether this occurred via autophagy has not been tested (Araki et al, 2009; Turner et al, 2011).
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