Aging Cell最新文献

RETRACTION: Chen, L., Yang, R., Qiao, W., Zhang, W., Chen, J., Mao, L., Goltzman, D., Miao, D. (2019). 1,25-Dihydroxyvitamin D exerts an antiaging role by activation of Nrf2-antioxidant signaling and inactivation of p16/p53-senescence signaling. Aging Cell, 18(3), e12951. https://doi.org/10.1111/acel.12951

The above article, published online on 24 March 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between; the journal Editor-in-Chief, Monty Montano; The Anatomical Society; and John Wiley & Sons Ltd. The retraction has been agreed due to duplications observed between elements of Figures 1h and 1j; 5d and 5f; 3a and 6j; and Supplemental Figures 4c and 4e.

The authors acknowledged their errors in figure management, which led to the duplications observed between Figures 3a and 6j, as well as between S4c and S4e. They also admitted to copying and pasting small areas from figure S4e into the same image for aesthetic purposes. Additionally, they admitted to editing Figure 4d (ChIP gel image) to reduce noise and enhance the clarity of the bands shown. The authors provided some data and an explanation for the similarities observed between Figures 1h and 1j; and Figures 5d and 5f. However, their explanation was not sufficient. Due to the extent of the identified issues, the editors have lost confidence in the data presented. The authors disagree with the retraction.

Usage of the phrase “biological age” has picked up considerably since the advent of aging clocks and it has become commonplace to describe an aging clock's output as biological age. In contrast to this labeling, biological age is also often depicted as a more abstract concept that helps explain how individuals are aging internally, externally, and functionally. Given that the bulk of molecular aging is tissue-specific and aging itself is a remarkably complex, multifarious process, it is unsurprising that most surveyed scientists agree that aging cannot be quantified via a single metric. We share this sentiment and argue that, just like it would not be reasonable to assume that an individual with an ideal grip strength, VO₂ max, or any other aging biomarker is biologically young, we should be careful not to conflate an aging clock with whole-body biological aging. To address this, we recommend that researchers describe the output of an aging clock based on the type of input data used or the name of the clock itself. Epigenetic aging clocks produce epigenetic age, transcriptomic aging clocks produce transcriptomic age, and so forth. If a clock has a unique name, such as our recently developed epigenetic aging clock CheekAge, the name of the clock can double as the output. As a compromise solution, aging biomarkers can be described as indicators of biological age. We feel that these recommendations will help scientists and the public differentiate between aging biomarkers and the much more elusive concept of biological age.

Cover legend: The cover image is based on the Article Cellular senescence by loss of Men1 in osteoblasts is critical for age-related osteoporosis by Yuichiro Ukon et al.,https://doi.org/10.1111/acel.14254

Cover legend: The cover image is based on the Article Accumulation of DNA G-quadruplex in mitochondrial genome hallmarks mesenchymal senescence by Kangkang Yu et al.,https://doi.org/10.1111/acel.14265

Cover legend: The cover image is based on the Article The SASP factor IL-6 sustains cell-autonomous senescent cells via a cGAS-STING-NFκB intracrine senescentnoncanonical pathway by Florencia Herbstein et al., https://doi.org/10.1111/acel.14258

Cover legend: The cover image is based on the Article Rejuvenation of the reconstitution potential and reversal of myeloid bias of aged HSCs upon pH treatment by Sachin Kumar et al.,https://doi.org/10.1111/acel.14324

Melendez, J., Sung, Y.J., Orr, M., Yoo, A., Schindler, S., Cruchaga, C., Bateman, R. Aging Cell, 2024. https://doi.org/10.1111/acel.14230

In the published version of Melendez et al. (2024), an incorrect version of Table 1 was shown.

The correct table is shown below.

We apologize for this error.

Although most drugs currently approved are meant to treat specific diseases or symptoms, it has been hypothesized that some might bear a beneficial effect on lifespan in healthy older individuals, outside of their specific disease indication. Such drugs include, among others, metformin, SGLT2 inhibitors and rapamycin. Since 2006, the UK biobank has recorded prescription medication and mortality data for over 500′000 participants, aged between 40 and 70 years old. In this work, we examined the impact of the top 406 prescribed medications on overall mortality rates within the general population of the UK. As expected, most drugs were linked to a shorter lifespan, likely due to the life-limiting nature of the diseases they are prescribed to treat. Importantly, a few drugs were associated with increased lifespans, including notably Sildenafil, Atorvastatin, Naproxen and Estradiol. These retrospective results warrant further investigation in randomized controlled trials.

Chronic sterile inflammation contributes to aging-associated pathologies/malignancies like cancer and autoimmune disorders. In their recent Nature article, Widjaja et al. established the pro-inflammatory, pro-fibrotic cytokine 11 (IL11) as a regulatory driver/hub of aging-associated inflammation (inflammaging) in mice. Genetic and pharmacological IL11 blockade reduces inflammaging, improving healthspan, lifespan, and longevity in male and female mice, highlighting IL11 as a new inflammatory aging clock and a potential molecular target in inflammaging-associated human degenerative diseases.

Nicotinamide adenine dinucleotide (NAD⁺) depletion has been postulated as a contributor to the severity of COVID-19; however, no study has prospectively characterized NAD⁺ and its metabolites in relation to disease severity in patients with COVID-19. We measured NAD⁺ and its metabolites in 56 hospitalized patients with COVID-19 and in two control groups without COVID-19: (1) 31 age- and sex-matched adults with comorbidities, and (2) 30 adults without comorbidities. Blood NAD⁺ concentrations in COVID-19 group were only slightly lower than in the control groups (p < 0.05); however, plasma 1-methylnicotinamide concentrations were significantly higher in patients with COVID-19 (439.7 ng/mL, 95% CI: 234.0, 645.4 ng/mL) than in age- and sex-matched controls (44.5 ng/mL, 95% CI: 15.6, 73.4) and in healthy controls (18.1 ng/mL, 95% CI 15.4, 20.8; p < 0.001 for each comparison). Plasma nicotinamide concentrations were also higher in COVID-19 group and in controls with comorbidities than in healthy control group. Plasma concentrations of 2-methyl-2-pyridone-5-carboxamide (2-PY), but not NAD⁺, were significantly associated with increased risk of death (HR = 3.65; 95% CI 1.09, 12.2; p = 0.036) and escalation in level of care (HR = 2.90, 95% CI 1.01, 8.38, p = 0.049). RNAseq and RTqPCR analyses of PBMC mRNA found upregulation of multiple genes involved in NAD⁺ synthesis as well as degradation, and dysregulation of NAD⁺-dependent processes including immune response, DNA repair, metabolism, apoptosis/autophagy, redox reactions, and mitochondrial function. Blood NAD⁺ concentrations are modestly reduced in COVID-19; however, NAD⁺ turnover is substantially increased with upregulation of genes involved in both NAD⁺ biosynthesis and degradation, supporting the rationale for NAD+ augmentation to attenuate disease severity.