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Using a multivariate genome-wide association study approach, the authors identified 52 genetic variants associated with aging-related traits, many of which are promising cardiometabolic targets that could promote healthy aging and inform future interventions.
Heterochronic parabiosis ameliorates age-related diseases in mice, but how it affects epigenetic aging and long-term health was not known. Here, the authors show that in mice exposure to young circulation leads to reduced epigenetic aging, an effect that persists for several months after removing the youthful circulation.
Adipose tissue has an important role in metabolic homeostasis and undergoes age-related changes contributing to metabolic decline, via mechanisms that remain incompletely explored. Here the authors show that Crtc2 deficiency in adipocytes protects against age-related hyperactivation of the BCAA–mTORC1 axis and metabolic alterations.
Many age-related disorders, such as neurodegenerative diseases, are associated with protein misfolding. Here, the authors identify LONRF2 as a protein quality control ubiquitin ligase that is expressed in neurons and ubiquitylates misfolded TDP-43 and hnRNP M1 and show that loss of Lonrf2 in mice results in late-onset motor neuron degeneration, whereas its ectopic expression partially rescued the phenotypes observed in motor neurons derived from patients with amyotrophic lateral sclerosis.
Yeo and Zhou et al. profile whole-genome chromatin accessibility in different cell types of the adult neurogenic niche, which reveals a reversible decrease in the migration of proliferative neural stem cells in aged mice.
Shen, Gao and Luo et al. show that the epigenetic regulator Cxxc1 plays an important role in maintaining homeostasis and function of group 3 innate lymphoid cells that are involved and key in regulating intestinal immunity during aging.
Delval, Hantute-Ghesquier, Sencio and colleagues demonstrate that depletion of age-associated senescent cells decreases pulmonary viral load and ameliorates early and late lung COVID-19 in a hamster model of aging.
Solá, Mereu and colleagues describe a chronic inflammatory state in the aging mouse skin that is characterized by IL-17 production by dermal lymphoid cells and demonstrate the potential of inhibition of IL-17 signaling in protection against skin aging.
Regulatory T (Treg) cells have an important role in age-related diseases and inflammation; however, the underlying mechanisms are not fully understood. Li et al. identify a Treg-specific long noncoding RNA, Altre, that binds Yin Yang 1 to regulate liver Treg mitochondrial function in old mice. Altre deletion accelerates aging-associated liver pathogenesis.
Seegren et al. demonstrate that the mitochondrial calcium uptake complex is a key molecular apparatus that links age-related changes in mitochondrial physiology to systemic macrophage-mediated age-associated inflammation.
The mechanisms underlying the influence of aging on cancer are incompletely understood. Warde et al. establish a new model of age- and sex-dependent adrenal cancer. Their work uncovers a tumor-protective role for myeloid immune cells that is enhanced by androgens.
Although vaccination drops COVID-19 mortality in older adults, post-vaccine fatal COVID-19 in nursing home outbreaks was linked to Delta, Gamma and Mu variants, persistently detected in aerosols. Mortality was predicted by IFNB1 or age, ORF7a and ACE2 mRNAs.
Oocyte meiotic defects increase with age and contribute to decreased oocyte quality. Here the authors show that granulosa cell mevalonate pathway abnormalities contribute to aneuploidy during ovarian aging and that supplementation with mevalonate metabolites improves oocyte quality, providing a potential therapeutic strategy for promoting female reproductive longevity.
Telomere shortening is a hallmark of aging and genetic telomerase deficiency causes premature aging phenotypes and reduces lifespan. Here the authors show that gut-specific telomerase expression is sufficient to rescue aging phenotypes and extend the lifespan of telomerase-deficient zebrafish, as well as ameliorate signs of aging in wild-type animals.
Chronic inflammation is a sign of immune system aging. Here the authors show that T cells from older adults contribute to inflammation due to CISH-mediated enhanced proteasomal degradation of a component of the proton pump V-ATPase, resulting in reduced lysosome function and the release of mtDNA and other amphisomal content.
The authors characterized m6A dynamics in primate tissue aging and revealed a new role for the METTL3–m6A–NPNT axis in maintaining skeletal muscle homeostasis, thereby providing insight into the epitranscriptomic machinery underlying primate aging.
The gut microbiome is closely connected to health. Pang et al. explored the gut microbiome and aging in a large cohort of 297 centenarians. The study shows that the gut microbiome in centenarians has a Bacteroides-enriched enterotype and youth-associated features.
Technologies could aid active and healthy aging but their development and implementation requires knowledge of user preferences. In this study, the authors conducted a Swedish national survey across three generations to understand attitudes toward technologies.
Moderate cold temperature extends lifespan, but the mechanisms involved are not fully understood. Here, the authors show that moderate cold temperature eliminates aggregation-prone proteins through PSME3-activated proteasomes in both C. elegans and human cells.
Sen et al. show that, during human cellular senescence and mouse tissue aging, chromatin alterations promote the initiation of transcription from non-canonical sites and lead to deterioration of cellular health.