Hallmarks of Aging Library
Every article, presentation, spotlight, and news item we've tagged to Hallmarks of Aging.
Showing 97–120 of 401
KIF14 Loss Drives Egg Aging Through Energy Failure
Declining levels of the kinesin protein KIF14 impair egg cell quality during reproductive aging by disrupting both the cellular scaffold and mitochondrial function. This mechanism reveals a specific molecular pathway linking reproductive senescence to energy production failure, with direct implications for fertility outcomes across the reproductive lifespan.
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.
Microglial Aging: How Transposable Elements Drive Neuroinflammation
Microglia, the brain's immune cells, show distinct patterns of transposable element activity across aging and Alzheimer's disease that differ markedly from whole-brain tissue. Transposable element transcripts remain stable through most of the human lifespan, then increase in late life, while autophagy and lysosomal function appear to regulate this activity—suggesting a previously unrecognized mechanism linking cellular housekeeping to neuroinflammatory aging.
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.
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.
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.
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.
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.
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.
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.
Social Connection Slows Aging Through Measurable Biology
Positive psychosocial exposures—joy, belonging, purpose, and social connection—function as biologically meaningful determinants of aging rates, operating through inflammatory, autonomic, and neuroendocrine pathways. The JoyScore Experiment quantifies these experiences using wearable neurotechnology and epigenetic markers, revealing preliminary evidence that active engagement in collective experiences correlates with slower biological aging trajectories.
TFEB Restores Autophagic Defense in Aging Kidneys
Aging impairs the kidney's autophagic response to toxic stress, leaving older individuals vulnerable to acute kidney injury. Restoring TFEB-mediated autophagy through pharmacological intervention partially reverses this age-related vulnerability in cellular models.
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.
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.
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.
Adipose RNA Control Preserves Metabolic Flexibility in Aging
A long noncoding RNA called Lncbate1 regulates lipid synthesis in white adipose tissue during aging by modulating a microRNA-protein axis. This molecular mechanism reveals how aging alters fat storage and mobilization, with implications for metabolic decline and age-related disease prevention.
Ammonia Dysregulation: Liver Aging's Systemic Cascade
Hepatic ammonia metabolism declines with age through mitochondrial dysfunction and disrupted metabolic regulation, compromising the liver's capacity to maintain nitrogen homeostasis and triggering inflammatory and fibrogenic remodeling. This pathway represents a mechanistic link between liver aging and systemic dysfunction across multiple organ systems.
SIRT3 blocks trained immunity, halting stem cell aging
SIRT3 suppression of hematopoietic stem cell aging prevents the development of trained immunity — a maladaptive immune memory state that drives chronic inflammation and tissue dysfunction. This mechanism directly links stem cell aging to the inflammatory cascade underlying age-related disease.
Isolation Triggers Inflammatory Oxylipin Surge in Aging
Social isolation in aged mice triggers a substantial increase in lipoxygenase-derived oxylipins, pro-inflammatory lipid mediators that amplify systemic inflammation. This finding establishes a direct biochemical pathway linking psychological stress to accelerated aging through altered lipid metabolism and immune dysregulation.
A Decline in Follicle Cell Function Is a Major Driver of Drosophila Ovarian Aging
Follicle cell dysfunction drives ovarian aging in Drosophila through accumulated defects in tissue integrity, genome stability, and germ-soma communication. Enhancing autophagy specifically in follicle cells restores reproductive capacity with age, indicating that somatic cell function is a critical lever in reproductive longevity.
Restoring Lysosomal Clearance Targets Parkinson's Root Cause
Researchers identified a protein that restores lysosomal clearance of alpha-synuclein, the pathogenic protein driving Parkinson's disease. This addresses a fundamental breakdown in cellular protein quality control that accelerates neurodegeneration with age.
MLKL-Driven Mitochondrial Stress Amplifies Senescence in Aging Liver
Hepatocyte MLKL accumulation in aging livers drives mitochondrial dysfunction and cellular senescence independent of necroptosis, amplifying inflammatory signaling across liver tissue through paracrine mechanisms. This identifies MLKL as a direct molecular driver of liver aging with potential therapeutic relevance to metabolic liver disease progression.
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.
Peripheral Inflammation Drives Brain Pathology via Vesicles
Peripheral inflammation triggered by aging or Parkinson's-associated mutations spreads to the brain via circulating extracellular vesicles, potentially driving neurodegeneration. This pathway reveals a previously unclear mechanism linking systemic inflammation to brain-specific pathology in age-related neurological disease.