Aging Cell最新文献

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.

Cover legend: The cover image is based on the article Single-cell transcriptomic atlas of taste papilla aging by Yiqun Yu et al., https://doi.org/10.1111/acel.14308.

Cover legend: The cover image is based on the article E5 treatment showing improved health-span and lifespan in old Sprague Dawley rats by Kavita Singh et al.,https://doi.org/10.1111/acel.14335.

A list of this decade's most prominent names in ageing research would undoubtedly include many women who have led the field in recent years. While the field, and science in general, still have far to go in achieving gender parity in opportunities and recognition, we can celebrate the progress made to date. However, the longer ‘history of the field’ that many of us present in our classrooms, conference halls and writings often tends to be dominated by men. Although numerous men have made fundamental observations that have shaped our understanding of ageing from both a mechanistic and evolutionary perspective, the unfortunate reality is that women making similar contributions have not received equal recognition throughout much of our field's history. As a starting point for wider representation and further conversations in this area, we present here a short list of women—Marjory Warren, Lillian Jane Martin, Margaret Alexander Ohlson, Rebeca Gerschman and Marion J. Lamb—whose contributions were foundational to ageing research in the 20th century. Their work spanned theoretical, experimental and clinical insight into the biology of ageing—and yet their names are too seldom mentioned when introducing our field. We hope this list can be a starting point for a more inclusive recognition of the diverse scientists who helped pave the way for our field today.

Senescent osteocytes are key contributors to age-related bone loss and fragility; however, the impact of mechanobiological changes in these cells remains poorly understood. This study provides a novel analysis of these changes in primary osteocytes following irradiation-induced senescence. By integrating subcellular mechanical measurements with gene expression analyses, we identified significant, time-dependent alterations in the mechanical properties of senescent bone cells. Increases in classical markers such as SA-β-Gal activity and p16^Ink4a expression levels confirmed the senescence status post-irradiation. Our key findings include a time-dependent increase in cytoskeletal Young's modulus and altered viscoelastic properties of the plasma membrane, affecting the contractility of primary osteocytes. Additionally, we observed a significant increase in Sclerostin (Sost) expression 21 days post-irradiation. These biophysical changes may impair osteocyte mechanosensation and mechanotransduction, contributing to bone fragility. This is the first study to time-map senescence-associated mechanical changes in the osteocyte cytoskeleton. Our findings highlight the potential of biophysical markers as indicators of cellular senescence, providing more specificity than traditional, variable biomolecular markers. We believe these results may support biomechanical stimulation as a potential therapeutic strategy to rejuvenate aging osteocytes and enhance bone health.

Prior studies have shown that interrupting the growth hormone/insulin-like growth factor-I (GH/IGF-I) signaling axis extends laboratory mouse lifespan, but confounding effects of additional gene or hormone deficiencies that exist in commonly used models of GH/IGF-I interruption obscure the specific effect of GH on longevity. We address this issue by using mice with a specific knockout of the GH gene and show that both males and females on a mixed genetic background display extended lifespans resulting from GH deficiency. Our physiological assessment of these mice revealed that in addition to weighing significantly less and displaying significantly greater body fat (as a percentage of body weight), GH deficient mice display significant impairments in glucose metabolism and preferential fat utilization. These data provide strong evidence that GH deficiency is directly responsible for the altered nutrient utilization and extended lifespan that is commonly observed in mouse models of GH/IGF-I interruption.

Lukasiewicz CJ, Tranah GJ, Evans DS, et al. Higher expression of denervation-responsive genes is negatively associated with muscle volume and performance traits in the study of muscle, mobility, and aging (SOMMA). Aging Cell. 2024;23(6):e14115. https://doi.org/10.1111/acel.14115

In Table 1 of the publication, the “Total Summary” value for 400 m walk speed is reported as 1.9 ± 0.2; however, it should be 1.1 ± 0.2.

We apologize for this error.

Cover legend: The cover image is based on the Article Age-related alterations in human cortical microstructure across the lifespan: Insights from high-gradient diffusion MRI by Hansol Lee et al., https://doi.org/10.1111/acel.14267