Editor-in-Chief: Monty Montano
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Aging Cell is an open access geroscience journal publishing research addressing the biology of aging. The journal welcomes research that reports the mechanistic, molecular, and cellular aspects of the aging process, as well as the links between aging and age-related disease.
With global readership, Aging Cell is a journal of The Anatomical Society and John Wiley and Sons, Ltd.
Aging Cell Best Paper Prize 2022
Rilmenidine extends lifespan and healthspan in Caenorhabditis elegans via a nischarin I1-imidazoline receptor
Dominic F. Bennett, Anita Goyala, Cyril Statzer, Charles W. Beckett, Alexander Tyshkovskiy, Vadim N. Gladyshev, Collin Y. Ewald, João Pedro de Magalhães
Aging Cell, Volume 22, Issue 2, February 2023, Pages 1-15Accepted Dec 09, 2022. First published: 20 January 2023
Aging Cell Joint Runner-Up Best Paper Prize
A single short reprogramming early in life initiates and propagates an epigenetically related mechanism improving fitness and promoting an increased healthy lifespan
Quentin Alle, Enora Le Borgne, Paul Bensadoun, Camille Lemey, Nelly Béchir, Mélissa Gabanou, Fanny Estermann, Christelle Bertrand-Gaday, Laurence Pessemesse, Karine Toupet, Romain Desprat, Jérôme Vialaret, Christophe Hirtz, Danièle Noël, Christian Jorgensen, François Casas, Ollivier Milhavet, Jean-Marc Lemaitre
Aging Cell, Volume 21, Issue 11, November 2022, Pages 1-12Accepted Aug 31, 2022. First published: 17 October 2022
Previous Awards of Aging Cell Best Paper Prize
Anatomical Society Research Studentships 2023/24
NEW RESEARCH STUDENTSHIPS 2023/24 - AWARDED FOR START DATE 01.10.24
Award of Anatomical Society Studentships
We are seeking applications from the Anatomical Society Membership for the 2023/24 round (student start date 1st October 2024). Application details can be found here. Click here to read more about the 2023/24 Research Studentships.
Articles
Enabling translational geroscience by broadening the scope of geriatric care
-  1 December 2023
Graphical Abstract

Translational Geroscience poses that slowing down the underlying mechanisms of aging will result in prevention of most diseases and disabilities that affect older persons. To facilitate this transformation will require a closer collaboration and wider discussion between gerontologists who study aging in research laboratories (geroscience) and geriatricians who maintain life course records and care for older patients with complex multimorbidity and disability (geriatric care). Figure generated using Office suite and Biorender.
Polygenic risk for schizophrenia, social dispositions, and pace of epigenetic aging: Results from the Young Finns Study
-  29 November 2023
Graphical Abstract

Individuals with a high polygenic risk for schizophrenia seem to display accelerated epigenetic aging at higher (vs. lower) inner drive for social relationships. A rather opposite pattern was found among those with a low polygenic risk for schizophrenia. Thus, frequent social interactions may relate to accelerated epigenetic aging in individuals at risk for psychosis.
Endothelial cell‐specific reduction in mTOR ameliorates age‐related arterial and metabolic dysfunction
-  28 November 2023
Graphical Abstract

Although systemic mTOR inhibition improves age-related physiological dysfunction, the cell types that mediate the beneficial effects remain elusive. Here, we demonstrate that endothelial cell-specific reduction of mTOR ameliorates arterial and metabolic function in old age. These improvements are concomitant with reduced senescence burden, inflammation, and oxidative stress in arteries, lung, adipose tissue, and liver. These results support the exploration of therapeutic strategies targeting endothelial mTOR signaling.
SIRT2 transgenic over-expression does not impact lifespan in mice
-  27 November 2023
Sirtuin 2 (SIRT2) has been implicated in cell cycle regulation, genome stability and neurodegeneration, and its over-expression in BubR1 hypomorph progeroid mice extends lifespan. Here, comprehensive phenotyping in male and female, chow and high fat fed mice shows no impact of SIRT2 over-expression on healthspan or lifespan on a non-progeroid, wild-type background.

The following is a list of the most cited articles based on citations published in the last three years, according to CrossRef.
The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs
-  644-658
-  9 March 2015
Senescence‐associated β‐galactosidase is lysosomal β‐galactosidase
-  187-195
-  17 March 2006
Identification of a novel senolytic agent, navitoclax, targeting the Bcl‐2 family of anti‐apoptotic factors
-  428-435
-  29 December 2015
Oxidative stress in the aging substantia nigra and the etiology of Parkinson's disease
-  20 August 2019
Graphical Abstract

Dopamine neurons within the healthy human substantia nigra exhibit mild oxidative stress during aging, resulting from their unique biochemical properties and a number of age-dependent biochemical changes specific to this neuronal population (grey). An exacerbation of these pathways, combined with additional environmental toxins and genetic mutations, worsens redox balance within nigral dopamine neurons in Parkinson's disease, causing excessive oxidative stress and dopamine neuron death (red).
Fat tissue, aging, and cellular senescence
-  667-684
-  16 September 2010