Aging-US

There may be many paths that lead to the cessation of aging, or there may only be one—this mystery has yet to reveal itself. However, there is a wide array of evidenced methods capable of preserving youth by slowing down the aging process, and even mildly reversing it. Some known natural interventions are healthy diets, consistent exercise and avoiding aging-related risk factors, including carcinogens such as alcohol, cigarettes and excess sun exposure. Researchers have also studied less intuitive repetitive behaviors that appear to improve the cognitive decline associated with aging. For example, in a study published in 2015, researchers found that active singing led to cognitive improvements in participants with dementia. “People engaging in lifelong music-making have been found to have better cognitive outcomes later in life.” In a research study published in 2020, 30 researchers—from National University of Singapore, Singapore Institute for Clinical Sciences, National University Health System, University of Cambridge, University of London, Singapore Immunology Network, Maurine Tsakok Inc, Voices of Singapore Choral Society, Presbyterian Community Services, NTUC Health Co-operative Limited, Beijing Chui Yang Liu Hospital, Fudan University, Massachusetts General Hospital, Harvard Medical School, Nanyang Technological University, Imperial College London, and Genome Institute of Singapore—conducted the world’s first study designed to compare the impact of choral singing versus health education on cognitive function and aging in a randomized controlled trial (RCT). Their trending research paper was published by Aging (Aging-US) and entitled, “Effects of choral singing versus health education on cognitive decline and aging: a randomized controlled trial”. “In this RCT, we hypothesized that choral singing would improve cognitive health and/or reduce cognitive decline in elderly with high risk of dementia.” Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-can-singing-improve-aging/ Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.202374 DOI - https://doi.org/10.18632/aging.202374 Full Text - https://www.aging-us.com/article/202374/text Correspondence to: Lei Feng email: pcmfl@nus.edu.sg Keywords: choral singing, health education, cognitive decline, biological markers, randomized controlled trial About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at http://www.Aging-US.com​​ or connect with us on: SoundCloud - https://soundcloud.com/aging-us​ Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging​ Pinterest - https://www.pinterest.com/AgingUS/ Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

The researchers recruited healthy older participants to two groups according to their history of tea drinking frequency and investigated both functional and structural networks to reveal the role of tea drinking on brain organization. The suppression of hemispheric asymmetry in the structural connectivity network was observed as a result of tea drinking. The authors did not observe any significant effects of tea drinking on the hemispheric asymmetry of the functional connectivity network. Dr. Junhua Li and Dr. Lei Feng said, "Tea has been a popular beverage since antiquity, with records referring to consumption dating back to the dynasty of Shen Nong (approximately 2700 BC) in China." Tea is consumed in diverse ways, with brewed tea and products with a tea ingredient extremely prevalent in Asia, especially in China and Japan. Although individual constituents of tea have been related to the roles of maintaining cognitive abilities and preventing cognitive decline, a study with behavioural and neurophysiological measures showed that there was a degraded effect or no effect when a constituent was administered alone and a significant effect was observed only when constituents were combined. The superior effect of the constituent combination was also demonstrated in a comparative experiment that suggested that tea itself should be administered instead of tea extracts; a review of tea effects on the prevention of Alzheimers disease, found that the neuroprotective role of herbal tea was apparent in eight out of nine studies. It is worth noting that the majority of studies thus far have evaluated tea effects from the perspective of neurocognitive and neuropsychological measures, with direct measurement of brain structure or function less-well represented in the extant literature. These studies focusing on brain regional alterations did not ascertain tea effects on interregional interactions at the level of the entire brain. The Li/Feng Research team concluded, "In summary, our study comprehensively investigated the effects of tea drinking on brain connectivity at both global and regional scales using multi-modal imaging data and provided the first compelling evidence that tea drinking positively contributes to brain structure making network organization more efficient." Full Text - https://www.aging-us.com/article/102023/text Correspondence to: Junhua Li email: junhua.li@essex.ac.uk and Lei Feng email: pcmfl@nus.edu.sg Keywords: tea drinking, brain efficiency, fMRI, DTI, default mode network, hemispheric asymmetry About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways. To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM

Aging-US published a Special Collection on Eye Disease which included "Activation of C-reactive protein proinflammatory phenotype in the blood retinal barrier in vitro: implications for age-related macular degeneration" which reported that the retinal pigment epithelium (RPE) is considered one of the main targets of age-related macular degeneration (AMD), the leading cause of irreversible vision loss among the ageing population worldwide. Increased levels of circulating pentameric C-reactive protein (pCRP) are associated with higher risk of AMD. Monomeric form of pCRP has been detected in drusen, the hallmark deposits associated with AMD, and we have found that mCRP induces oBRB disruption Dr. Blanca Molins from The IDIBAPS, Hospital Clínic de Barcelona said, "Age-related macular degeneration (AMD) is the primary cause of irreversible vision loss among the ageing population worldwide." AMD presents RPE cell abnormalities, disruption of the outer blood-retinal-barrier (oBRB), and degeneration of photoreceptors. Altered immune responses are thought to contribute to the dry AMD phenotype. Loss of parainflammation control contributes to AMD by invoking a chronic, heightened immune response that causes tissue destruction. mCRP has been identified in ocular drusen and other subepithelial deposits, as well as in the choroid, and contributes to oBRB disruption in vitro. The "non-risk" Factor H (FH) variant can effectively bind to mCRP to dampen its proinflammatory activity. MCRP levels are elevated in individuals with the high-risk CFH genotype [29, 30] - this is because there is no CRP transcription in retinal tissue. The Molins Research Team concluded in their https://www.aging-us.com/article/103655/ Aging-US Research Output, "our findings further support mCRP direct contribution to progression of AMD, at least at the RPE level. The topological experiments elicit that mCRP is proinflammatory when present on the apical side of the RPE. However, mCRP is likely to only reach the apical side of the RPE in compromised RPE health and where barrier functions are compromised. Thus, a plausible scenario would infer that, in the presence of an already aged/damaged RPE, mCRP reaches the apical side of the RPE to amplify the proinflammatory microenvironment and enhance barrier disruption. With respect to previous findings, this pathologic mechanism will be more prevalent in patients carrying the FH risk polymorphism for AMD, where mCRP proinflammatory effects remain unrestrained." Full Text - https://www.aging-us.com/article/103655/text Correspondence to: Blanca Molins email: bmolins@clinic.cat Keywords: age-related macular degeneration, retinal pigment epithelium, inflammation, C-reactive protein About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways. To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM

Aging-US published a Special Collection on Eye Disease which included "Loss of macroH2A1 decreases mitochondrial metabolism and reduces the aggressiveness of uveal melanoma cells" which reported that uveal melanoma (UM) is the most common primary intraocular tumour in adults. Most accurate prognostic factor of UM is classification by gene expression profiling. These authors recently showed a strong prognostic role of the expression levels of histone variant macroH2A1 in UM patients. Mitochondrial function was assayed through qPCR and HPLC analyses. Correlation between mitochondrial gene expression and cancer aggressiveness was studied using a bioinformatics approach. Dr. Giovanni Li Volti and Dr. Manlio Vinciguerra said, "Uveal melanoma (UM) is the most common primary intraocular tumour in adults." Metastasis is a frequent occurrence in uveal and cutaneous melanomas with a 5 years survival of 15%. By far the most common site of UM metastasis is the liver, reported in 87% of cases. Epigenetic mechanisms controlling gene expression have long been known to have a role in cancer development. In UM these include DNA methylation at CpG islands leading to decrease expression of p16/INK4a tumour suppressor protein. The Volti/Vinciguerra Research Team concluded in their Aging-US Research Output, "we suggest that strategies aiming at decreasing the expression of histone variant macroH2A1 [32], might effectively hamper the aggressiveness of UM cells, by inhibiting their mitochondrial phosphorylation. This could be a novel promising therapeutic strategy against UM [51]." Full Text - https://www.aging-us.com/article/103241/text Correspondence to: Giovanni Li Volti email: livolti@unict.it and Manlio Vinciguerra email: manlio.vinciguerra@fnusa.cz Keywords: macroH2A1, histones, uveal melanoma, metabolism, epigenetics About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways. To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM

Aging-US published a Special Collection on Eye Disease which included "Role of Citicoline in an in vitro AMD model" which reported that citicoline is the exogenous form of the nootropic, Cytidine 5'-diphosphate-choline that exerts its neuroprotective effects in the brain as well as in the eye. Citicoline alleviates apoptotic effects as evidenced by diminished AnnexinV/PI and Caspase-3/7 staining, downregulation of apoptosis genes, enhanced cell viability, and reduced oxidative stress in AMD RPE cybrid cells. However, further studies are required to establish the merit of citrusoline as a cytoprotective molecule in AMD and to decipher the molecular underpinnings of its mechanism of action. Dr. M. Cristina Kenney from The University of California Irvine said, "Citicoline is the international nonproprietary name given to the exogenous pharmacological form of Cytidine 5'-diphosphate-choline (CDP-Choline, CDPCho), a naturally occurring endogenous nucleotide compound that is water-soluble and has a molecular weight of 488.32 g/mol" Citicoline maintains neuronal membrane integrity, influences neurotransmitter levels, increases norepinephrine and dopamine levels in the central nervous system, restores the activity of membrane sodium/potassium ATPase and mitochondrial ATPase, and enhances brain function. Owing to these mechanisms, it has been successfully used as a neuroprotective agent to prevent neuronal aging and improve memory and learning in vitro. It has been extensively used in preclinical studies and clinical trials for neurodegenerative diseases including Parkinson's disease and glaucoma. This in vitro study supports our hypothesis as Citicoline conferred significant protection against apoptotic cell death that was in-part mediated by damaged mtDNA from AMD patients. The Kenney Research Team concluded in their Aging-US Research Output, "although further studies with Citicoline/ AMD RPE cybrid cells are underway, these results present novel findings that identify Citicoline to be a potential protector that attenuates apoptotic cell death in AMD. Citicoline is available as an over-the-counter dietary supplement in the U.S. and offers the advantage of easy access that shortens considerably the transition from lab bench to clinic." Full Text - https://www.aging-us.com/article/103164/text Correspondence to: M. Cristina Kenney email: mkenney@uci.edu Keywords: Citicoline, age-related macular degeneration (AMD), neuroprotection, RPE, mitochondria About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways. To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM

Will you age quickly or slowly? Is it possible to predict how long you will live based on your genetics, lifestyle and other traits? In a new study, a team of researchers—from the National Institutes of Health’s National Institute on Aging, University of California San Diego, University of Michigan, Consiglio Nazionale delle Ricerche, Azienda Sanitaria di Firenze, and ViQi, Inc.—sought to answer these questions by developing a novel framework designed to estimate human physiological age and aging rate. Their trending paper was published by Aging (Aging-US) in October 2021, and entitled, “Predicting physiological aging rates from a range of quantitative traits using machine learning”. “We present machine learning as a promising framework for measuring physiological age from broad-ranging physiological, cognitive, and molecular traits.” Full blog - https://www.mishablagosklonny.com/2021/11/05/trending-with-impact-machine-learning-predicts-human-aging/ Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.203660 DOI - https://doi.org/10.18632/aging.203660 Full Text - https://www.aging-us.com/article/203660/text Correspondence to: Luigi Ferrucci email: ferruccilu@grc.nia.nih.gov, David Schlessinger email: schlessingerd@grc.nia.nih.gov, Ilya Goldberg email: ilya@viqi.org and Jun Ding email: jun.ding@nih.gov Keywords: physiological aging rate, quantitative trait, machine learning, aging clock, mortality, personalized medicine About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at http://www.Aging-US.com​​ or connect with us on: SoundCloud - https://soundcloud.com/aging-us​ Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging​ Pinterest - https://www.pinterest.com/AgingUS/ Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Aging-US published a Special Collection on Eye Disease which included "Systemic administration of the di-apocarotenoid norbixin (BIO201) is neuroprotective, preserves photoreceptor function and inhibits A2E and lipofuscin accumulation in animal models of age-related macular degeneration and Stargardt disease" which reported that atrophic A\age-related macular degeneration and Stargardt disease are major blinding diseases affecting millions of patients worldwide - but no treatment is available. Acute and chronic retinal degeneration following blue light damage in BALB/c mice and aging of Abca4-/- Rdh8-/- mice, respectively, reproduce features of AMD and STGD. Norbixin injected intraperitoneally in BALB/c mice, maintained scotopic and photopic electroretinogram amplitude and was neuroprotective. Dr. Serge Camelo from The Sorbonne Université said, "Age-related macular degeneration (AMD) is the commonest cause of severe visual loss and blindness in developed countries among individuals aged 60 and older." AMD is a major unmet medical need as it is estimated that more than 20 million patients will be affected by 2050 in the US alone. STGD is the most common hereditary macular dystrophy, mostly affecting young patients aged between 6 and 15 years old with a prevalence of 1/8,000-1/10,000. It has an autosomal recessive mode of inheritance and may lead to registered blindness within the second or third decade of life. It is formed by the reaction of 2 all-trans retinal molecules with phosphatidylethanolamine generating N-retinylidene-PE, as a detoxication mechanism of retinal isomers including all-trans and 11-cis-retinal. Under normal conditions the ABCA4 protein participates in the elimination of A2-PE from the photoreceptors and inhibition of this clearance increases the accumulation of A2E and all-trans-retinal dimer in the RPE. Recently, it has been shown that ABCA4 is also expressed in RPE cells where it would participate in the recycling of retinaldehyde released during proteolysis of rhodopsin in endolysosomes following phagocytosis of photoreceptor outer segments. Indeed, it has been shown that as early as in 3-month-old Abca4-/- Rdh8-/- mice, the amplitudes of scotopic A and B waves and flicker ERG are reduced. Abca4-/- Rdh8-/- mice recapitulate most phenotypic retinal alterations observed during STGD and AMD, and represent a chronic model of these diseases. Acute white-light exposure is known to induce apoptosis of photoreceptors in albino mice retinas. The Camelo Research Team concluded in their Aging-US Research Output, "our present study demonstrates that systemic administration of norbixin in the acute BLD model of dry AMD is neuroprotective and partially preserves photoreceptor function. In addition, 6 months of oral supplementation with norbixin is effective in Abca4-/-Rdh8-/- mice. We show that chronic norbixin supplementation reduces the concentration of A2E in the eye, that norbixin is neuroprotective, and preserves visual function of Abca4-/-Rdh8-/- mice, modelling retinal degenerative conditions such as STGD and dry AMD. We believe that treatment using norbixin could potentially preserve “night” and “day” visual acuity in humans affected by dry AMD and STGD. It is essential for patient care to develop drugs that are effective on visual function following oral administration rather than by repeated local intraocular injections. These results demonstrated the effectiveness of the norbixin in a chronic and acute model of retinal degeneration and could offer a new therapeutic strategy, alone or in combination with gene therapies, for AMD and/or STGD patients. Thus, norbixin is a good drug candidate to treat patients and may provide a cure for these very debilitating diseases." Full Text - https://www.aging-us.com/article/103014/text Correspondence to: Serge Camelo email: serge.camelo@biophytis.com Keywords: norbixin, retinal function, A2E, AMD, Stargardt disease

Aging-US published "Effects of estradiol on biological age measured using the glycan age index" which reported that glycan age is a recently developed biomarker based on glycans attached to immunoglobulin G. In large population cohorts, glycan age associates well with lifestyle and disease-risk biomarkers, while some studies suggested that glycan changes precede development of several age-associated diseases. In this study the authors evaluated effects of estrogen on the glycan age. After the recovery period glycan age returned to baseline values in both groups. These results suggest that IgG glycans and consequently also the glycan age are under strong influence of gonadal hormones and that estradiol therapy can prevent the increase of glycan age that occurs in the perimenopausal period. Dr. Gordan Lauc from The Genos Glycoscience Research Laboratory as well as The University of Zagreb said, "The existence of inter-individual differences in the pace of biological aging is an intriguing concept that tries to explain why some people stay healthy until very late chronological age, while other people age faster and have a shorter life expectancy." A number of biomarkers aimed at an objective estimation of biological age have been developed in the past several years, one of them being the glycan age, which is based on analyzing glycans attached to immunoglobulin G. A key feature of a good biomarker of biological age is that the difference between chronological and biological age should correlate with known biomarkers of an unhealthy lifestyle and that increased biological age should predict future disease development. Glycans attached to IgG change significantly with age and have been suggested as a promising biomarker of biological age. Furthermore, since glycosylation affects interactions between IgG and different Fc receptors and other ligands, changes in glycosylation have direct effects on the function of the immune system, with multiple functional implications. IgG glycans have been shown to be a reliable biomarker of aging that explains up to 64% of variation in chronological age. However, IgG glycans are not only biomarkers but also functional effectors that participate in the process of aging. This prevented the calculation of glycan age from the available data since glycan age is based on IgG glycans. Aiming to evaluate the effects of ovarian sex hormone suppression followed by estradiol supplementation on biological age measured by the glycan age these authors reanalysed samples from the same intervention study using state of the art glycoprofiling technology. The Lauc Research Team concluded in their Aging-US Research Output that recently a modest improvement in epigenetic age was reported in a small group of individuals undertaking quite radical pharmacological intervention and glycan age was shown to slightly improve by exercise. However, all these changes were modest compared to the effects of the suppression of gonadal hormones, which more than doubled glycan age in some of the participants. Sign up for free Altmetric alerts about this article DOI - https://doi.org/10.18632/aging.104060 Full Text - https://www.aging-us.com/article/104060/text Correspondence to: Gordan Lauc email: glauc@pharma.hr Keywords: biological age, glycan age, estrogen, aging biomarkers, glycosylation About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways. To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl

Aging-US published a Special Collection on Eye Disease which included "Immunological analyses reveal an immune subtype of uveal melanoma with a poor prognosis" which reported that uveal melanoma is an aggressive intraocular malignancy that often exhibits low immunogenicity. Metastatic uveal Melanoma samples frequently exhibit monosomy 3 or BAP1 deficiency. In this study, the authors used bioinformatic methods to investigate the immune infiltration of uveal melanoma samples in public datasets. The Kaplan-Meier method and log-rank test were used to assess the prognostic value of particular immune cells and genes in samples. These authors used CIBERSORT and ESTIMATE with RNA-seq data from The Cancer Genome Atlas and the GSE22138 microarray dataset to determine the sample-level immune subpopulations. Dr. Zhaoyang Wang and Dr. Xianqun Fan said, "Immune heterogeneity within the tumor microenvironment has been linked to the drug sensitivity and prognosis of patients with various cancer types." Profiling of immune signatures might uncover biomarkers for targeted therapy and clinical outcome assessment. Uveal melanoma (UM) is the most common aggressive intraocular malignancy in adults, and originates from the uveal tract. Monosomy 3 tumors were found to be enriched for genes in immune pathways such as interferon signaling, T cell invasion and cytotoxicity. Mutation of GNA11/GNAQ was not found to significantly alter the immune infiltration and HLA Class I expression in UM patients. Characterizing the immunological features of UM may provide novel immune biomarkers for prognostic assessment and immunotherapy. Enhancing the cytolytic functions of infiltrating lymphocytes can significantly improve antitumor immunity. However, due to the low levels of cytotoxic cells in the tumor microenvironment, non-responsiveness to immunotherapy remains a clinical challenge. The Wang/Fan Research Team concluded in their Aging-US Research Output that gene expression profiling of UM patients treated with immune checkpoint blockers has advanced the application of genomic data to tumor immunology. The authors hope that large sequencing data from UM patients undergoing immune checkpoint blocker treatment will emerge in the future. The immune features reported herein should be considered for integration into prognostic models or explored as predictors of adjuvant immune therapy responsiveness in patients with BAP1-deficient UM. The Volti/Vinciguerra Research Team concluded in their Aging-US Research Output, "we suggest that strategies aiming at decreasing the expression of histone variant macroH2A1 [32], might effectively hamper the aggressiveness of UM cells, by inhibiting their mitochondrial phosphorylation. This could be a novel promising therapeutic strategy against UM [51]." Full Text - https://www.aging-us.com/article/102693/text Correspondence to: Zhaoyang Wang email: zhaokekewzy@hotmail.com and Xianqun Fan email: fanxq@sjtu.edu.cn Keywords: immune subtype, uveal melanoma, bioinformatics, immune cell fractions, TCGA About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways. To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM

Iron is a mineral naturally found in the environment on Earth, within food sources and in all living organisms. A number of biochemical systems require this mineral and, in humans, the lack of iron results in anemia and a deficiency in hemoglobin—the protein responsible for supplying the body with oxygen. Anemia can also be caused by iron dysregulation. This occurs when iron damages the protein it should be safely stored in, such as ferritin, and then reacts in a toxic manner with surrounding cellular structures and organs. While iron is essential, the chemical properties of iron can make it a harmful substance if it is not tightly regulated. “The very property of iron that makes it useful, its ability to accept or donate electrons, also gives it the ability to damage molecules and organelles via the Fenton reaction, in which iron reacts with hydrogen peroxide, leading to the formation of the highly reactive and toxic free radical, hydroxyl.” Dennis Mangan (P. D. Mangan) is a clinical biochemist/microbiologist, researcher, author, health and fitness expert, and anti-aging specialist. In October of 2021, he authored a new theory article that positions iron as a potential driver of aging. This trending paper was published in Aging (Aging-US) Volume 13, Issue 19, and entitled, “Iron: an underrated factor in aging.” Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-is-iron-a-driver-of-aging/ Press Release - https://www.aging-us.com/news_room/iron-an-underrated-factor-in-aging Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.203612 DOI - https://doi.org/10.18632/aging.203612 Full Text - https://www.aging-us.com/article/203612/text Correspondence to: Dennis Mangan email: pdmangan@outlook.com Keywords: iron, aging, oxidative stress, calorie restriction, plasma dilution About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at http://www.Aging-US.com​​ or connect with us on: SoundCloud - https://soundcloud.com/aging-us​ Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging​ Pinterest - https://www.pinterest.com/AgingUS/ Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM