Hallmarks of Aging Library

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Showing 49–72 of 225

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.

Wiley Aging CellFeb 26, 2026

Intergenerational Transmission of Metabolic Changes in Oocytes From Aged Mice

Oxidative stress in oocytes from aged female mice triggers lipid accumulation and metabolic alterations that persist through three generations, with offspring developing compensatory antioxidant responses in lipid-rich tissues. This demonstrates that maternal aging imprints metabolic dysfunction on descendants independent of direct genetic mutation.

Wiley Aging CellFeb 11, 2026

Architect of Frailty Biology and Champion of Translational Geroscience

Jeremy Walston's work established frailty as a biologically coherent condition rooted in chronic inflammation, mitochondrial dysfunction, and impaired stress responsiveness rather than inevitable aging. His translational research framework has advanced clinical intervention strategies and shaped how geroscience addresses loss of physiologic reserve across aging populations.

Wiley Aging CellMar 31, 2026

A Cluster of Three snoRNAs Including Jouvence Required in the Gut Determines Lifespan and Confers Neuroprotection Through Metabolic Parameters

A cluster of three small nucleolar RNAs in the gut epithelium regulates lipid and sterol metabolism, with direct effects on lifespan and neuroprotection in aging. Disruption of these snoRNAs causes metabolic dysregulation that leads to neurodegeneration, while restoration in gut cells alone is sufficient to reverse these effects.

Nature - npj AgingMar 20, 2026

Mitorubin, berberrubine-based compounds that improve mitochondrial function, exhibit cardioprotective effects against age-related cardiac dysfunction

Mitorubin, a berberrubine-derived compound, restores mitochondrial function and protects cardiac tissue from age-related deterioration. This addresses a primary mechanism of cardiovascular aging by targeting energy production capacity at the cellular level.

Wiley Aging CellMar 25, 2026

Senescence‐Driven IL‐17A Inflammatory Circuit Promotes Epithelial–Mesenchymal Transition (EMT) and Progression in Age‐Related Posterior Subcapsular Cataracts

Senescent lens epithelial cells drive posterior subcapsular cataracts through an IL-17A inflammatory loop that activates NF-κB signaling, triggering epithelial-mesenchymal transition and accelerated tissue remodeling. This positions age-related cataracts as a senescence-driven pathology rather than a protein aggregation problem, with implications for understanding how cellular aging propagates through tissues.

Nature - npj AgingApr 6, 2026

HCCaging: a liver physiological aging-related biomarker for hepatocellular carcinoma diagnosis based on transcriptome data

Researchers identified HCCaging, a transcriptome-based biomarker that reflects liver aging patterns and improves hepatocellular carcinoma diagnosis. This tool bridges the gap between cellular aging processes and cancer risk stratification, offering earlier detection potential before advanced disease.

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