Aging Cell最新文献

Cover legend: The cover image is based on the article Skeletal muscle mitochondrial fragmentation predicts age-associated decline in physical capacity by Rob Wüst et al., https://doi.org/10.1111/acel.14386.

The establishment of various molecular, physiological, and genetic markers for cellular senescence and aging-associated conditions has progressed the aging study. To identify such markers, a combination of optical, proteomic-, and sequencing-based tools is primarily used, often accompanying extrinsic labels. Yet, the tools for clinical detection at the molecular, cellular, and tissue levels are still lacking which profoundly hinders advancements in the specific detection and timely prevention of aging-related diseases and pathologies. Raman spectroscopy, with its capability for rapid, label-free, and non-invasive analysis of molecular compositions and alterations in aging cells and tissues, holds considerable promise for in vivo applications. In this review, we present recent advancements in the application of Raman spectroscopy to the study of aging in cells and tissues. We explore the use of Raman spectroscopy and related techniques for detecting cellular aging and senescence, focusing on the molecular alterations that accompany these processes. Subsequently, we provide a review of the application of Raman spectroscopy in identifying aging-related changes in various molecules within tissues and organs.

Liu, H., Xu, Q., Wufuer, H., Li, Z., Sun, R., Jiang, Z., Dou, X., Fu, Q., Campisi, J., Sun, Y. (2024). Rutin is a potent senomorphic agent to target senescent cells and can improve chemotherapeutic efficacy. Aging Cell 23(1): e13921.

In Figure 5e, for SA-β-Gal staining of mouse tissues, the Placebo image was mistakenly picked up to make the original panel. The corrected figure is provided below.

We apologize for this error.

Multimodal study of Alzheimer's disease (AD) dorsolateral prefrontal cortex (DLPFC) showed AD-related aberrant intron retention (IR) and proteomic changes not observed at the RNA level. However, the role of sex and how IR may impact the proteome are unclear. Analysis of DLPFC transcriptome showed a clear sex-biased pattern where female AD had 1645 elevated IR events compared to 80 in male AD DLPFC. Increased IR is correlated with lower mRNA levels, suggestive of nonsense-mediated mRNA decay. Two hundred thirty-three mRNAs with elevated IR in females were curated AD genes enriched for ubiquitin-like protein ligase and Tau protein binding. Increased IR genes in combined sex and female AD cohorts showed significant changes in their protein expression patterns with 11%–24% of them differential expressed proteins (DEP), alluding to the regulation of AD proteome by IR independent of RNA level. Upregulated DEPs in male AD were linked to RNA splicing that may prevent aberrant IR, whereas in female AD, they overlapped significantly more with the MAPK/metabolism module associated with cognitive decline. IR genes appeared to be significantly downregulated in specific female AD inhibitory and excitatory neurons compared to control. Differentially retained introns in female AD have elevated H3K27ac marks, strong CTCF binding at their flanking exons, and enriched for PABPC1 motif. Given that H3K27ac is repressive over gene bodies in aged brain and CTCF impedes transcription elongation, their binding patterns can delay co-transcriptional recruitment of spliceosome to cause IR, which may in turn contribute to different trajectories of AD pathology in women.

Cover legend: The cover image is based on the article A longevity-specific bank of induced pluripotent stem cells from centenarians and their offspring by George Murphy et al., https://doi.org/10.1111/acel.14351.

Cover legend: The cover image is based on the article Altered tubulin detyrosination due to SVBP malfunction induces cytokinesis failure and senescence, underlying a complexhereditary spastic paraplegia by Aurora Pujol et al., https://doi.org/10.1111/acel.14355.

Cover legend: The cover image is based on the article Organellar quality control crosstalk in aging-related disease: Innovation to pave the way by Gu He et al.,https://doi.org/10.1111/acel.14447.

From embryogenesis to aging, billions of cells perish daily in mammals. The multistep process by which phagocytes engulf these deceased cells without eliciting an inflammatory response is called efferocytosis. Despite significant insights into the fundamental mechanisms of efferocytosis, its implications in disorders such as aging and cancer remain elusive. Upon summarizing and analyzing existing studies on efferocytosis, it becomes evident that efferocytosis is our friend in resolving inflammation, yet it transforms into our foe by facilitating tumor development and metastasis. This review illuminates recent discoveries regarding the emerging mechanisms of efferocytosis in clearing apoptotic cells, explores its connections with aging, examines its influence on tumor development and metastasis, and identifies the regulatory factors of efferocytosis within the tumor microenvironment. A comprehensive understanding of these efferocytosis facets offers insights into crucial physiological and pathophysiological processes, paving the way for innovative therapeutic approaches to combat aging and cancer.

Organellar homeostasis and crosstalks within a cell have emerged as essential regulatory and determining factors for the survival and functions of cells. In response to various stimuli, cells can activate the organellar quality control systems (QCS) to maintain homeostasis. Numerous studies have demonstrated that dysfunction of QCS can lead to various aging-related diseases such as neurodegenerative, pulmonary, cardiometabolic diseases and cancers. However, the interplay between QCS and their potential role in these diseases are poorly understood. In this review, we present an overview of the current findings of QCS and their crosstalk, encompassing mitochondria, endoplasmic reticulum, Golgi apparatus, ribosomes, peroxisomes, lipid droplets, and lysosomes as well as the aberrant interplays among these organelles that contributes to the onset and progression of aging-related disorders. Furthermore, potential therapeutic approaches based on these quality control interactions are discussed. Our perspectives can enhance insights into the regulatory networks underlying QCS and the pathology of aging and aging-related diseases, which may pave the way for the development of novel therapeutic targets.

Cover legend: The cover image is based on the article Cooperative nuclear action of RNA-binding proteins PSF and G3BP2 to sustain neuronal cell viability is decreased in aging anddementia by Satoshi Inoue et al., https://doi.org/10.1111/acel.14316.