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Senescent cells and their production of inflammatory cytokines (senescence-associated secretory phenotype) affects aging and disease, including cancer. Zhang et al. report that epigenomic remodeling by KDM4 controls the senescence-associated secretory phenotype, and KDM4 expression by stromal cells of the tumor microenvironment promotes prostate cancer.
Arthur et al. report the biochemical and proteomic (SomaLogic) profiling of plasma and CyTOF immunophenotyping of peripheral blood mononuclear cells from 71 individuals with COVID-19 or other inflammatory pulmonary diseases, and 148 healthy donors aged 25–80 years old. The Resource reveals unique determinants of COVID-19 disease relative to healthy aging and other pulmonary disorders.
Aging, inflammation and senescence are controlled by NFκB. Cai and Han identify by comparative genomics a family of lncRNAs that are increasingly expressed during aging by NFκB-driven transcription, and find that many of these aging-associated lncRNAs regulate NFκB activity in turn.
In a cohort of older men from the Veterans Affairs Normative Aging Study, exposure to fine particulate matter (PM2.5), over just a few weeks and under levels considered hazardous, was found to impede cognitive function in older adults, but the adverse effects were lessened in people taking nonsteroidal anti-inflammatory drugs.
The authors show that exosomal transfer of osteoclast-derived microRNAs to chondrocytes decreases the resistance of cartilage to matrix degeneration, angiogenesis and sensory innervation, and promotes osteoarthritis progression in mice.
Aging is accompanied by structural and functional alterations of the central nervous system (CNS). Here, the authors show that cytotoxic CD8+ T cells accumulate in the CNS during normal aging, leading to axonal damage and contributing to age-related cognitive and motor decline.
Microglia can help clear amyloid β plaques in the Alzheimer’s disease brain but may also become dysfunctional and can contribute to disease progression. March-Diaz et al. reveal that hypoxia, a potentially modifiable risk factor for Alzheimer’s disease, disrupts the metabolism and function of microglia near plaques, which may contribute to neuropathology.
Using genetic and demographic data from the UK Biobank, the authors clustered 116 common diseases based on their age-of-onset profiles and found increased genetic similarity within clusters, suggesting common etiologies. Two of the four disease clusters were associated with aging-related genes but differed in functional enrichment and evolutionary profiles.
This study demonstrates that short and dysfunctional telomeres sensitize kidneys to develop fibrosis and enhance the genetic program associated with epithelial-to-mesenchymal transition in two mouse models of kidney fibrosis.
The authors found that the olfactory perception of food abundance can regulate the impact of dietary restriction on longevity in Caenorhabditiselegans. They show that food odors act on olfactory circuitry that signals the gut via octopamine to suppress dietary restriction-induced longevity.
Ito et al. show that regeneration in the aging brain is impaired due to reduced expression of the apelin receptor APJ. Circulating apelin signals oligodendrocytes via APJ to support remyelination, and this pathway can be restored in older mice with an APJ agonist.
A cohort study tracking 20-year age-related declines in multiple organ systems finds that, already by midlife, those aging fastest showed cognitive declines, signs of brain aging, diminished sensory–motor function and negative views about aging.
The authors present a small noncoding RNA atlas characterizing two longitudinal Parkinson’s disease cohorts and reveal potential biomarkers for disease detection, their relation to molecular hallmarks of PD and regulatory disease-progression modules.
The authors identify an atypical type of stem cell division that regulates hair follicle organ homeostasis and aging in mice. These ‘stress-responsive-type’ asymmetrical cell divisions cause hair follicle stem cells to detach from the basement membrane leading to their exhaustion, elimination and organ aging.
In a nationwide, longitudinal and population-based matched-cohort study, Janbek and colleagues find dementia to be a risk factor for infection-related hospital contacts and conclude that infections might be an early sign of dementia.
Using a mouse model of lung fibrosis, the authors find that overexpression of SIRT3 in myofibroblasts lowers their threshold for apoptosis, allowing their clearance from tissues and restoration of the lost capacity for fibrosis resolution in aged mice.
The authors show that plasma levels of NfL increase with age in humans and are associated with mortality in nonagenarians and centenarians. In mice, a life-extending dietary restriction manipulation attenuated the similar age-related increase in plasma NfL levels.
Investigation of the long-lived blind mole rat adaptive immune system reveals that they do not accumulate large memory T-cell clones and effector programs with aging. Such organization could relieve the burden of inflammaging triggered by persistent clonal expansions and contribute to the long and healthy Spalax lifespan.
Stressed mitochondria activate multiple defense pathways to improve health. Li et al. show that the acetyltransferases CBP/p300 play a central role in mitochondrial stress signaling that defends mitochondrial function and promotes health and longevity.
Using metagenomics sequencing, Zhang et al. examined sex- and age-dependent trajectories of the gut microbiota in four cohorts across China, Israel and the Netherlands. The authors found age-related gut microbial trajectories common across all populations, with the abundance of Streptococcus gordonii predicting chronological age.