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Han et al. provide a substantial contribution to our limited comprehension of the mechanisms of aging in adipose tissue. They show that, with age, increased levels of adipose CRTC2 decrease the breakdown of branched-chain amino acids and activate mTORC1. This in turn leads to increased levels of senescence-associated secretory phenotype factors, which promotes senescence and adipose dysfunction.
Neuronal aging is highly associated with misfolded protein aggregates that predispose to neurodegeneration, but the cellular factors that are involved in removing misfolded proteins are yet to be identified. In this issue of Nature Aging, Li and colleagues identified LONRF2 as an important player in protecting aging neurons against the accumulation of protein aggregates.
Aging increases vulnerability to respiratory viral infections, including by SARS-CoV-2. Delval et al. established a causal role for age-related pre-existing senescent cells in the severity of COVID-19 symptoms in an aging hamster model. Selective depletion of senescent cells using senolytic agents mitigated the risk of severe COVID-19 symptoms linked to aging.
Warde and colleagues demonstrate sex-specific differences in senescence in the adrenal glands of aged mice, with males eliciting a more robust, protective myeloid response that is associated with protection from adrenal cancer.
Li and colleagues address the effect of regulatory T (Treg) cells on the aging process and the role of long non-coding RNAs in Treg cell function. They show that a Treg cell-specific and age-induced long non-coding RNA, Altre, protects the aging liver from age-related apoptosis and metabolic abnormalities.
Liu and colleagues investigate the effects that ovarian aging may have in granulosa cell-to-oocyte communication and demonstrate that oocyte rejuvenation and the extension of reproductive lifespan is possible by increasing lipid metabolism in granulosa cells in mouse.
The mysteries behind immune aging and its related inflammation are being unmasked. Jin et al. reveal that the defective turnover of damaged mitochondria in CD4+ T cells from older individuals results in the exacerbated secretion of mitochondrial DNA, which fuels inflammaging and impairs immune responses.
Epigenetic changes are a driver of senescence and occur during aging. A study in Nature Aging shows how chromatin-mediated loss of transcription fidelity, previously shown in yeast and worms, also occurs in mammalian cells and could constitute a new hallmark of senescence and aging.
The ability of adult neural stem cells to produce new neurons (neurogenesis) declines markedly during aging, but exactly how this occurs is largely unknown. Using sophisticated in vivo imaging, a study in Nature Aging shows that aging affects several steps of neurogenesis — most notably, increasing the death of newborn clones.
Wang Lin and his colleagues explore how aging reprograms spatially unique pathways in liver endothelial cells to cause fibrosis. They find that loss of KIT in liver endothelial cells close to the central vein upregulates the chemokine receptor CXCR4 to stimulate inflammation, enhance fibrosis and increase lipid accumulation in aged liver.
Aging is known to be associated with a decline in memory and mood, but the molecular mechanisms that underlie these changes remain unclear. Moigneu, Abdellaoui and colleagues show that growth differentiation factor 11 reverses deficits in these functions in aged mice, pointing the way towards a novel pro-mnemonic and antidepressant therapeutic target.
Zhang and colleagues demonstrate how the premature aging phenotypes in progeria involve a mitotic spindle-assembly-checkpoint protein, BUBR1. BUBR1 is misanchored to the nuclear membrane by progerin and its mRNA is destabilized in progeria, preventing it from functioning properly.
Aging is known to exacerbate atherosclerosis, but the mechanisms have been largely unknown. A study in Nature Aging reveals a bone-marrow-controlled axis of clonality during atherosclerosis, showing that aged bones drive an inflammatory milieu that promotes smooth muscle polyclonality and the formation of larger lesions.
Mating is known to accelerate the aging of the opposite sex in a variety of species. A transcriptomic analysis of extracted germlines from mated and unmated Caenorhabditis elegans by Shi and Murphy now identifies a Piwi-interacting RNA-to-Hedgehog signaling pathway that regulates the accelerated aging of hermaphrodites.
There are no current standard-of-care treatments for sarcopenia, an age-associated decline in muscle mass and strength. A new study shows that genetically or pharmacologically countering the age-associated accumulation of sphingolipids in skeletal muscle can ameliorate sarcopenia in mice. The authors also identify genetic variants linked to sphingolipid biosynthesis that associate with muscle function in aged humans.
In our aging global population and with no effective treatments, the cognitive impairments associated with Alzheimer’s disease represent a major healthcare problem. A recent study in Nature Aging highlights intermittent fasting as a potential way to decrease the progression of Alzheimer’s disease in mice through changes to the gut microbiota.
Aging is associated with an accumulation of myeloid-biased hematopoietic stem cells with reduced regenerative potential, but the underlying mechanisms remain unclear. A study by Wendorff et al. demonstrates that inactivation of a single epigenetic regulator — the plant homeodomain factor 6 (PHF6) — transcriptionally and functionally rejuvenates mouse aged hematopoietic stem cells.
A new study shows that decreased cystatin A synthesis in aged epidermis mediates age-related bone loss, whereas topical treatment that restores cystatin A mitigates this loss. This report demonstrates that skin aging has systemic consequences by showing that signals originating in skin can control bone function.
Elder abuse has been recognized as a serious problem for decades. Yet rigorous studies are rare. Burnes and colleagues move the field forward by identifying how pervasive the problem is, the factors that increase and decease vulnerability, and how these factors change over a three-year period.
While C. elegans males are known to induce demise of hermaphrodites, the mechanism underlying this phenomenon is poorly understood. Through transcriptomic analyses, Booth et al. identify specific hermaphrodite gene sets that respond to male pheromones, sperm and seminal fluid and can mediate premature death of hermaphrodites.
