Hallmarks of Aging Library

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Showing 49–72 of 239

Wiley Aging CellFeb 5, 2026

Lifespan and Fecundity Impacts of Reduced Insulin Signalling Can Be Directed by Mito‐Nuclear Epistasis in Drosophila

Reduced insulin signaling extends lifespan in Drosophila, but the effect—beneficial or detrimental—depends on the genetic interaction between mitochondrial and nuclear DNA. This reveals that conserved aging mechanisms operate differently across individuals based on mito-nuclear epistasis, with direct implications for personalized longevity interventions.

Nature AgingMar 20, 2026

Spontaneous aging-associated inflammation and genome instability in the immune system of turquoise killifish

Turquoise killifish demonstrate rapid, age-associated immune system deterioration marked by chronic inflammation, genomic instability, and functional decline. This model reveals how innate immune dysregulation accelerates aging trajectories in vertebrates, offering mechanistic insights applicable to understanding human immunosenescence.

Wiley Aging CellFeb 12, 2026

p62/SQSTM1 Condensation Modulates Mitochondrial Clustering to Participate in Mitochondrial Quality Control

p62 protein condensation drives clustering of damaged mitochondria during selective autophagy, acting as a quality control mechanism that slows mitochondrial turnover. ALS/FTD-associated mutations disrupt this clustering process, impairing the cell's ability to manage dysfunctional mitochondria—a hallmark of age-related neurodegeneration.

Nature - npj AgingApr 6, 2026

Biomarkers of oxidative damage as a tool to investigate frailty syndrome in older women

Oxidative damage biomarkers correlate with frailty in older women, providing measurable indicators of cellular stress that precede functional decline. Identifying these markers enables earlier intervention before frailty manifests clinically.

Wiley Aging CellFeb 15, 2026

Additional Cover

This research maps transcriptomic changes across multiple organs during aging in mice, revealing organ-specific and shared molecular signatures of senescence. Understanding these distinct aging patterns across tissues is fundamental to identifying intervention points for age-related decline.

LifeSpan.ioMar 3, 2026

Novel Mechanism for Parkinson’s Is Linked to ATP Deficiency

ATP deficiency impairs dopamine packaging into synaptic vesicles by reducing function of VMAT2, a transporter that requires ATP energy, leading to dopamine oxidation and α-synuclein accumulation characteristic of Parkinson's disease. This mechanism links mitochondrial dysfunction to neurodegeneration in human dopaminergic neurons and may explain both familial and sporadic disease pathology.

Wiley Aging CellApr 22, 2026

Comorbid Alzheimer's Disease and Type 2 Diabetes Microbiota Shape Age‐Associated Gut–Brain Axis Profiles

Microbiota from elderly donors with both Alzheimer's disease and type 2 diabetes produce the most severe dysbiosis when transplanted into mice, suppressing hippocampal neurotrophic gene expression through loss of butyrate-producing bacteria and enrichment of pro-inflammatory taxa. This demonstrates a direct mechanistic link between comorbid metabolic and neurodegenerative disease states and gut-brain axis dysfunction.

Wiley Aging CellMar 20, 2026

Issue Information

This issue of Aging Cell (Volume 25, Issue 4, April 2026) aggregates current research on cellular and organismal aging mechanisms. Without access to specific article abstracts or contents, the longevity relevance depends on the individual research papers included in this issue.

Wiley Aging CellFeb 24, 2026

Correction to “Spatial Reorganization of Chromatin Architecture Shapes the Expression Phenotype of Therapy‐Induced Senescent Cells”

This correction addresses a published study on how senescent cells reorganize their chromatin architecture in response to therapeutic stress. Understanding the structural changes in non-dividing cells has direct implications for improving cellular resilience and longevity through better therapeutic design.

LT WireApr 15, 2026

Anavex highlights shared autophagy biology in autism and Alzheimer’s

Anavex presents evidence linking autism spectrum disorder and Alzheimer's disease through impaired autophagy and synaptic dysfunction, proposing that restoring cellular clearance pathways via their compound Blarcamesine may address both conditions. The finding connects neurodevelopmental and neurodegenerative disease through a shared cellular mechanism, with epidemiological data showing autistic adults face substantially elevated dementia risk.

Longevity.TechnologyMar 17, 2026

Ternary raises $4.4m to fight inflammaging with AI drugs

Ternary Therapeutics raised $4.4 million to develop AI-designed molecular glues that selectively degrade or modulate proteins driving chronic inflammation and neuroinflammation. This approach addresses inflammaging, a fundamental aging process linked to age-related disease burden, through a closed-loop AI platform rather than conventional blocking mechanisms.

Wiley Aging CellApr 9, 2026

Single‐Cell Profiling Reveals RAB13+ Endothelial Cells and Profibrotic Mesenchymal Cells in Aged Human Bone Marrow

Single-cell analysis reveals that aging bone marrow undergoes distinct cellular remodeling: endothelial cells develop prothrombotic and mitochondrial dysfunction, while a novel RAB13+ arterial endothelial subset emerges alongside expansion of profibrotic mesenchymal cells. These cellular shifts directly impair the marrow's capacity to support healthy blood cell production and tissue maintenance, establishing specific molecular targets for intervention.

Nature AgingApr 6, 2026

Extracellular vesicles derived from senescent hepatocytes drive pan-cancer metastasis in aging

Senescent hepatocytes in aging release extracellular vesicles containing microRNAs that enhance metastatic potential across multiple cancer types in aged organisms. This mechanism directly links hepatic aging to systemic cancer progression, identifying a previously uncharacterized pathway connecting liver dysfunction to increased metastatic risk in older adults.

Wiley Aging CellFeb 25, 2026

Silencing of the Metabolic Gene HKDC1 Is Associated With Aging and Neurodegeneration in Mice and Humans

HKDC1, a metabolic enzyme, declines with age due to chromatin remodeling that blocks its transcription factor regulation, and this decline correlates with cognitive impairment and neurodegeneration in both mice and humans. Loss of HKDC1 compromises mitochondrial integrity and triggers neuroinflammation, establishing a mechanistic link between metabolic gene silencing and age-related neurological decline.

Wiley Aging CellApr 6, 2026

Senescent Factors Suppress Innate Antiviral Immunity in Aged Mice via Two Distinct Mechanisms

Senescent cells accumulate with age and suppress antiviral immunity through four secreted factors—GDF15, IGF1, IL1α, and IL6—via two distinct signaling pathways. Blocking these factors restores innate antiviral defense in aged mice, offering a mechanistic target to improve immune resilience against infection in older adults.

Nature AgingMay 12, 2026

Hypoxia-induced autophagic degradation of HIF-1α attenuates cellular aging and extends mammalian lifespan

Intervertebral discs age slowly due to selective autophagy of HIF-1α under naturally hypoxic conditions. A small molecule designed to replicate this mechanism across tissues may extend mammalian lifespan by modulating how cells respond to low-oxygen environments.

Nature - npj AgingMar 23, 2026

Dietary metabolomic determinants of frailty through inflammation in the Canadian Longitudinal Study on Aging

Specific dietary metabolites—compounds produced when the body processes food—predict frailty risk through inflammatory pathways in aging adults. This identifies measurable intermediate markers that connect diet composition to loss of physical function, a primary driver of morbidity and mortality in older populations.

LifeSpan.ioFeb 19, 2026

A Circulating Inflammation Suppressor Decreases Mortality

Mendelian randomization analysis demonstrates that elevated IL-6, a pro-inflammatory cytokine, causally increases mortality risk, while circulating IL-6 receptor (IL6R) decreases it. This identifies a specific inflammatory pathway amenable to therapeutic intervention in age-related mortality.

Wiley Aging CellMar 26, 2026

Differential Gene Expression in Human Hippocampus With Aging

Gene expression analysis of human hippocampal tissue reveals distinct molecular signatures in aging characterized by increased inflammation, reduced DNA repair capacity (particularly RAD23B), and altered neural activity patterns. RAD23B expression declines with age and is further reduced in Alzheimer's disease, positioning it as a relevant marker of hippocampal aging and neuronal vulnerability.

Nature AgingApr 10, 2026

Single-cell analysis of the human immune system reveals sex-specific dynamics of immunosenescence

Single-cell immune profiling across nearly 1,000 adults reveals sex-specific patterns of immune aging, with females demonstrating more extensive age-related remodeling of immune function. These findings establish a biological basis for observed sex differences in inflammatory disease prevalence and infection susceptibility across the lifespan.

Nature AgingMar 10, 2026

Simultaneous spatial transcriptomics and morphology profiling as tools to explore how microglia change with age

Microglia—the brain's resident immune cells—exhibit distinct transcriptional patterns and morphological changes with age, with subcellular mRNA localization directly influencing their functional capacity. This work establishes how aging alters the molecular foundation of neuroinflammation, a process central to cognitive decline and neurodegenerative disease progression.

Wiley Aging CellMay 8, 2026

Correction to “Monoamine Oxidase‐A Is a Novel Driver of Stress‐Induced Premature Senescence Through Inhibition of Parkin‐Mediated Mitophagy”

This correction addresses methodological refinements in research demonstrating that monoamine oxidase-A drives stress-induced cellular aging by disrupting the cell's ability to clear damaged mitochondria. The finding clarifies a direct mechanism linking stress response dysfunction to accelerated senescence at the mitochondrial level.

Wiley Aging CellFeb 13, 2026

Telomere Shortening Drives Atrial Fibrillation Through VCAM‐1 Mediated Atrial Electrical and Structural Remodeling

Telomere shortening drives atrial fibrillation through VCAM-1 upregulation, which promotes atrial fibrosis and electrical dysfunction. Blocking VCAM-1 reverses these changes and reduces AF susceptibility by 30%, identifying a mechanistic pathway linking cellular aging to arrhythmia risk.

Wiley Aging CellMar 30, 2026

Pck1 Deficiency Drives Mitochondrial Dysfunction and Cellular Senescence in Adipocytes

Pck1 deficiency in adipocytes impairs mitochondrial function, causing fumarate accumulation that triggers oxidative stress, mtDNA release, and chronic inflammation—a mechanism linking metabolic dysfunction to aging. This identifies a targetable pathway in the progression of age-related metabolic disease.

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