Aging & Longevity
500 peer-reviewed studies indexed
NAT10 Promotes Tubular Epithelial Cell Senescence in Cisplatin-Induced Acute Kidney Injury by Regulating DDX17.
NAT10 promotes cisplatin-induced renal tubular cell senescence via DDX17 upregulation, suggesting that targeting the NAT10/DDX17 signaling axis may offer a potential therapeutic strategy for AKI.
Brain aging in bipolar disorder using a neuroimaging and machine learning-derived metric: Findings from the ENIGMA BD Working Group.
BD was associated with higher brain-PAD compared to HC primarily among older patients, with AED use related to more advanced brain age while lithium use alone or in combination was not associated with advanced brain age, suggesting a possible neuroprotective effect of lithium.
Personality and cognitive resilience to accelerated epigenetic aging.
Personality traits (neuroticism, conscientiousness, and openness) are associated with cognitive resilience to accelerated epigenetic aging, with neuroticism linked to worse-than-expected cognition and conscientiousness and openness linked to better-than-expected cognition relative to epigenetic aging measures.
Novel PMVs/ZIP4/Zinc/Prelamin A Axis Promotes Nuclear Dysmorphism and Vascular Aging in Humans and Rodents Post-Injury: Effective Treatment With Platelet Membrane-Coated ZIF-8 Nanoparticles.
A novel PMVs/ZIP4/Zinc/Prelamin A axis promotes nuclear dysmorphism and vascular aging in injured human and rodent arteries, and platelet membrane-coated ZIF-8 nanoparticles effectively alleviate these effects through zinc supplementation.
Incarcerated geriatric patients' experiences of aging and healthcare.
Older adults incarcerated in a county jail experienced difficulty navigating the physical jail environment due to aging and unaddressed disabilities, and faced numerous challenges accessing healthcare including procedural opacity, mutual distrust with medical staff, and reliance on serendipity for successful care.
Senescence-induced endothelial-to-mesenchymal transition accelerates the subretinal fibrosis in neovascualr age-related macular degeneration.
The accumulation of senescent endothelial cells promotes subretinal fibrosis via endothelial-to-mesenchymal transition in nAMD, and targeting these cells with senolytic treatment represents a promising therapeutic strategy for mitigating fibrosis-associated vision loss.
PFKFB3 nuclear translocation improves diabetic retinopathy by attenuating endothelial cell senescence through inhibition of USP7-p53 axis.
Nuclear PFKFB3 attenuates endothelial cell senescence in diabetic retinopathy by interacting with USP7 to constrain the USP7-p53 axis and promote proteasomal degradation of p53, suggesting that targeting PFKFB3 nuclear translocation may be a novel therapeutic strategy for diabetic retinopathy.
Perceived Normal and Pathological Aging? A Cross-cultural Comparison Between French and Congolese.
French participants rated aging situations more severely and better differentiated normal from pathological aging compared to Congolese participants, demonstrating that 'perception of normal or pathological behavior in aging is not universally shared across cultures.'
Reduced osteogenic factors and early osteoblast senescence in SOD1(G93A) ALS mouse model.
Bone deterioration precedes overt motor symptoms in SOD1(G93A) ALS mice and is linked to osteoblast premature senescence, reduced osteogenic factors, and early structural deficits independent of muscle denervation.
P2X7R deficiency alleviates cardiac senescence by enhancing mitophagy via the HuR/TRIM26/NR4A1 axis.
P2X7R deficiency alleviates cardiac senescence by enhancing mitophagy via the HuR/TRIM26/NR4A1 axis, whereby P2X7R promotes HuR nucleocytoplasmic shuttling to increase TRIM26 mRNA stability, leading to NR4A1 ubiquitination and proteasomal degradation that suppresses mitophagy and accelerates cardiac ageing.
BMAL1 downregulation exacerbates age-related nonalcoholic steatohepatitis by promoting NLRP3 inflammasome activation via HIF-1ɑ-mediated glycolysis.
BMAL1 downregulation under aging and HFD conditions promotes NASH progression by binding to HIF-1α and modulating the glycolysis-NLRP3 inflammasome axis.
Correspondence of large-scale functional brain network decline across aging mice and humans.
Resting-state functional MRI in awake mice reveals modular functional brain network organization that undergoes age-related dedifferentiation analogous to humans, while mouse networks are more segregated than human networks and decline at slower rates across the lifespan.
Senescent Synovial Intimal Fibroblasts Aggravate Osteoarthritis by Regulating Macrophage Polarization and Chondrocyte Phenotype Through ANGPTL4-α5β1 Axis.
Senescent synovial intimal fibroblasts aggravate osteoarthritis by promoting M1 macrophage polarization and cartilage degeneration through paracrine secretion of ANGPTL4 via the α5β1 integrin axis, with transcription factors EGR1 and ATF3 regulating senescence-related pathways in these cells.
Lactucopicrin promotes the autophagic degradation of MAP2K4/MKK4 by mediating CCDC50 palmitoylation to alleviate osteoarthritis progression.
Lactucopicrin alleviates osteoarthritis progression by enhancing ZDHHC4-catalyzed palmitoylation of CCDC50, which facilitates selective autophagic degradation of MAP2K4/MKK4, thereby suppressing MAPK/JNK signaling and chondrocyte senescence.
Triclosan exacerbates post-myocardial infarction injury via Nur77 ubiquitination: Linking NTRK2/PGC-1α-mediated mitochondrial dysfunction to senescence and ferroptosis.
TCS exacerbates post-MI injury by disrupting the Nur77/NTRK2/PGC-1α axis, triggering mitochondrial dysfunction-mediated ferroptosis and senescence in cardiomyocytes, and pharmacological activation of PGC-1α with ZLN005 represents a potential strategy to counteract TCS-induced adverse outcomes after MI.
Association of various insulin resistance surrogate indices with aging acceleration and future risk of cardiovascular disease in individuals with cardiovascular-kidney-metabolic syndrome stages 0-3: insights from CHARLS 2011-2020 data.
Multiple insulin resistance surrogate indices independently predict cardiovascular disease in CKM syndrome stages 0-3, with biological aging acceleration mediating 1.3-16.4% of the IR-CVD association.
Fenofibrate targets PPARα-CPT1C axis to reverse aging by regulating lipid metabolism and mitochondrial function.
Fenofibrate delays aging progression and reverses cellular senescence in a strictly PPARα-dependent manner by activating the PPARα-CPT1C axis to attenuate lipid accumulation and mitochondrial dysfunction in senescent cells and aged mice.
Sarcopenia as a causal mediator in aging, obesity and central obesity related outcomes: A comprehensive analysis of NHANES, CHARLS and ELSA.
Sarcopenia partially mediates age-related all-cause mortality and cardiovascular outcomes across three large cohorts, and modulates obesity-related outcomes variably across cohorts, suggesting sarcopenia prevention may reduce age- and obesity-associated health risks.
Piezo1-dependent activation of stromal cells ignites muscle inflammation in exercise and injury and is associated with inflammaging.
Piezo1-dependent mechanosensing by muscle mesenchymal stromal cells transduces exercise-induced mechanical stress into local inflammatory responses and is necessary for appropriately timed inflammatory and myogenic responses to acute muscle injury and is associated with age-related muscle inflammation.
Consensus document on frailty: conceptualization, detection, multidisciplinary management and future roadmap.
Frailty is the expression of an age-associated clinical phenotypic syndrome driven by the biology of aging, life-course environmental exposures, and disease burden, with its physiological basis lying in a heterogeneous decline of functional reserve across organ systems accompanied by impaired homeostasis and reduced capacity to respond to stressors.
OMICmAge quantifies biological age by integrating multi-omics with electronic medical records.
OMICmAge, a multi-omics biological age biomarker integrating epigenetic, proteomic, metabolomic, and clinical domains while remaining quantifiable from DNA methylation alone, is strongly associated with incident and prevalent chronic diseases and mortality, performing comparably or better than current biomarkers across discovery and validation cohorts.
Biological age acceleration associates with Alzheimer's disease plasma biomarker levels.
Biological age acceleration measured in blood in a Hispanic cohort enriched for preclinical individuals can stratify clinical AD risk and is associated with plasma AD biomarker levels.
ERRα-NOS2-mediated citrulline metabolism attenuates tubular epithelial cell senescence in diabetic kidney disease.
ERRα regulates NOS2-mediated citrulline metabolism to attenuate tubular epithelial cell senescence in diabetic kidney disease, and modulating ERRα and NOS2 activity may present a potential therapeutic strategy to reduce kidney injury and slow DKD progression.
Functional testosterone deficiency in aging men: Clinical impact, diagnostic pathways, and treatment strategies.
Guideline-directed testosterone therapy, when judiciously prescribed, can reverse many perturbations of hypogonadism while converging evidence including from recent large-scale randomized controlled trials demonstrates that modern testosterone therapy does not augment cardiovascular risk or mortality.
Single-cell atlas of human lung aging identifies cell type dyssynchrony and increased transcriptional entropy.
Lung aging is cell-type dyssynchronous, with alveolar epithelial and endothelial cells exhibiting the greatest transcriptional changes, increased somatic mutation burdens, and increased transcriptional entropy, while cells expressing commonly accepted senescence signatures did not increase with age.
Identifying Susceptibility Genes and Shared Genetic Architecture for Longevity and Muscle Weakness.
This study identified susceptibility genes for longevity (APOC1, TOMM40) and muscle weakness (DYM, TGFA) and uncovered shared pleiotropic loci linking aging and muscle decline, improving understanding of the genetic architecture underlying aging-related phenotypes.
Reduced glycoprotein hormone β5 links male aging and testosterone decline to increased adiposity.
GPHB5 is the 'missing' intermediary hormone linking testosterone (and aging) and its well-known catabolic effect on adipose tissue.
Molecular underpinnings of induced degenerative heterogeneity in the retinal pigment epithelium.
Cigarette smoke condensate induces epigenetic-mediated degenerative RPE heterogeneity characterized by globally decreased chromatin accessibility and dedifferentiated cell populations, with young RPE mounting compensatory upregulation of aging-related genes that aged RPE cannot, decreasing their survival.
GenX-associated molecular signatures overlap with testicular aging and male infertility: a multi-omics integration analysis.
SOD1, XRCC5, FOXO3, and POLB are candidate biomarkers for GenX-induced reproductive toxicity, with oxidative stress and genome maintenance as key pathological mechanisms.
Retinal and Choriocapillaris Thickness and Age in Macaques in Development and Aging.
Cynomolgus macaques undergo thickening of multiple retinal layers through their juvenile stage followed by thinning with age, and choriocapillaris thickness increases with age in both macaques and humans, suggesting remodeling due to aging.
Uncovering the signatures of aging and senescence in the human dorsolateral prefrontal cortex.
Spatial transcriptomics and single-nucleus RNA sequencing of nonpathological human dorsolateral prefrontal cortex revealed age-associated gene expression changes across cortical layers, altered cellular composition including increased homeostatic astrocytes and decreased SST inhibitory neurons, a decline in oxidative phosphorylation and cytoplasmic translation genes, oligodendrocyte senescence hallmarks with linear increases in CDKN2A, and enrichment of senescence-associated gene programs in white matter and layer 1 astrocyte and vascular cell populations.
Cellular circadian period and its deviation associate with Alzheimer's pathology and brain aging in cognitively impaired older adults.
Cellular circadian period and its deviation from 24 h capture distinct biological processes—AD-related tau pathology vs. broader aging-related neurodegeneration—and together represent complementary cellular biomarkers with potential prognostic value in older adults with cognitive concerns.
Evaluating the association of apolipoprotein E genotype and cognitive resilience in SuperAgers.
APOE allele frequency relates to SuperAger status, with NHW SuperAgers showing significantly lower APOE-ε4 and higher APOE-ε2 frequencies compared to cases and controls, while similar patterns in NHB SuperAgers did not consistently reach significance.
Silencing of the Metabolic Gene HKDC1 Is Associated With Aging and Neurodegeneration in Mice and Humans.
HKDC1 expression declines with aging and cognitive decline in humans and mice, and brain-specific knockout of HKDC1 in mice produces age-dependent anxiety, compromised memory and learning, senescence, neuroinflammation, and mitochondrial function deficits driven by reduced TFEB-mediated transcription due to chromatin conformation changes.
Healthy dietary patterns, longevity genes, and life expectancy: A prospective cohort study.
Five healthy dietary patterns were associated with lower all-cause mortality and 1.5 to 3.0 years of life gained at age 45, with associations remaining significant regardless of genetic susceptibility to longevity.
Magnesium Deficiency Accelerates Gut Aging and Increases Susceptibility to Colitis.
Magnesium homeostasis is identified as a key regulator of gut health, with age-related decline in gut magnesium levels accelerating intestinal aging and increasing susceptibility to colitis, while dietary magnesium intake of 334.7–420.0 mg/day confers significant protection against gut disorders in humans.
Opposite effects of chronic HIV infection and antiretroviral medication on organismal and organ-specific biological aging.
HIV infection accelerates systemic biological aging causally linked to inflammatory and metabolic complications, while specific antiretroviral drugs reduce age acceleration, revealing opposite effects of chronic HIV infection and antiretroviral medication on biological aging.
Establishing the relationship between brain cellular senescence and brain structure.
Cell-type-specific gene expression signatures linking brain structure and cellular senescence were identified in excitatory neurons and microglia, with associations observed across life stages suggesting mechanisms supporting brain development may also contribute to volume reduction observed during aging.
Cellular senescence in human liver under normal aging and cancer.
Profiling 43 normal human livers using single-cell multiome, spatial transcriptomics, and CODEX revealed cell-type-specific senescence programs associated with age, fibrosis, and cancer, with chemotherapy intensifying hepatocyte senescence 5-fold relative to aging and senescent cells sharing AP-1 activation, pro-inflammatory cytokines, and apoptosis resistance across conditions.
Relationship between locus coeruleus and slow-wave sleep in aging and Alzheimer's disease.
LC integrity, sex, and PVS burden show associations with SWS alterations in aging and AD, supporting restorative sleep as a potential therapeutic target.
Sertoli cell aging: damage accumulation and epigenetic alterations affecting male fertility.
Sertoli cells are the most sensitive testicular cell type to aging, displaying the highest number of aging-related differentially expressed genes and greatest increase in transcriptional noise, with progressive quantitative loss, morphological changes, and molecular damage collectively impairing male reproductive function.
Aging-caused the changes of the gut microbiota drive intestinal barrier dysfunction and increase sepsis susceptibility.
Aging-associated increases in Klebsiella aerogenes abundance drive elevated histamine production that exacerbates intestinal barrier dysfunction in sepsis by inhibiting Nlrp6 expression and its binding to LC3, thereby impairing autophagy.
CardioMetAge estimates cardiometabolic aging and predicts disease outcomes.
CardioMetAge, an aging clock constructed from chronological age and 12 common clinical biomarkers, outperformed existing aging clocks in predicting cardiometabolic disease mortality, incidence, and progression, and was slowed by two-year caloric restriction by 1.23 years relative to ad libitum control.
MTFR1L is a cardiac antiaging factor for maintenance of mitochondrial homeostasis.
MTFR1L is identified as a regulator of mitophagy that binds p-S65-Ub to amplify the PINK1/Parkin axis, and its progressive age-associated decline in the heart contributes to impaired mitochondrial homeostasis and accelerated cardiac dysfunction.
Integrative epigenetics and transcriptomics identify aging genes in human blood.
An integrative multi-omic approach combining epigenetic and transcriptomic data identifies aging genes in human blood that are enriched for adaptive immune functions, replicate more robustly across diverse populations, and are more strongly associated with aging-related outcomes compared to genes identified using either data type alone.
A cross-population compendium of gene-environment interactions.
A cross-population atlas of gene-environment interactions comprising 440,210 individuals from European and Japanese populations with replication in 539,794 individuals reveals how gene-environment interactions uncover missing heritability, affect polygenic prediction accuracy and cross-population portability, and identify sex-discordant genetic effects in lipid metabolism informing clinical trial failures.
Effects of daily multivitamin-multimineral and cocoa extract supplementation on epigenetic aging clocks in the COSMOS randomized clinical trial.
Daily multivitamin-multimineral supplementation modestly reduced the rate of increase of second-generation epigenetic clocks PCGrimAge and PCPhenoAge over 2 years, while cocoa extract had no effect on any of the five epigenetic clocks tested.
Targeting immune cells in the aged brain reveals that engineered cytokine IL-10 enhances neurogenesis and improves cognition.
An engineered IL-10 variant that uncouples pro- and anti-inflammatory responses positively impacted the transcriptome of multiple cell types, enhanced neurogenesis, and improved cognition in aged mice, paving the way for immunotherapies for the aged brain.
Liver exerkine reverses aging- and Alzheimer's-related memory loss via vasculature.
The liver-derived exerkine GPLD1 reverses aging- and Alzheimer's-related memory loss by targeting brain vasculature through cleavage of the GPI-anchored substrate TNAP, and inhibiting TNAP recapitulates cognitive benefits of GPLD1 in old age.
Heritability of intrinsic human life span is about 50% when confounding factors are addressed.
Heritability of human life span due to intrinsic mortality is above 50% when confounding by extrinsic mortality is corrected for, which is similar to heritability of most other complex human traits.