Hallmarks of Aging Library

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Showing 145–168 of 239

Longevity.TechnologyFeb 2, 2026

Why precision medicine is changing how we treat aging

Precision medicine approaches that integrate regenerative therapies, peptides, and personalized diagnostics address the cellular foundations of chronic pain and accelerated aging rather than managing symptoms alone. This shift from symptom suppression to root-cause intervention reflects an emerging understanding that dysfunction across multiple physiological domains—inflammation, energy production, cellular cleanup, and tissue regeneration—converges in conditions labeled as chronic pain or age-related decline.

Wiley Aging CellApr 9, 2026

Senolytic Treatment Reduces Acute and Chronic Lung Inflammation in an Aged Mouse Model of Influenza

Senolytic treatment with ABT-263 reduced lung and intestinal inflammation and prevented long-term pulmonary damage in aged mice infected with influenza, though it did not reduce viral replication itself. The findings indicate that pre-existing senescent cells drive inflammatory pathology rather than viral control, suggesting a therapeutic target for improving outcomes in older adults.

Wiley Aging CellApr 25, 2026

Long‐Term Stress Adaptation as a Highly‐Conserved Key Factor in Yeast Aging

Prolonged stress—distinct from acute stress—activates molecular pathways in yeast that recapitulate aging hallmarks including proteostasis collapse and epigenetic dysregulation. These changes are reversible upon stress relief, and the underlying genes are conserved across all life domains, suggesting aging may represent a maladaptive long-term stress response rather than passive damage accumulation.

LifeSpan.ioFeb 5, 2026

Increasing Senolytic Effectiveness by Stressing Mitochondria

Mitochondrial stress emerges as a critical mechanism underlying senolytic effectiveness against senescent cells. This finding suggests that the therapeutic benefit of senolytics depends partly on their capacity to induce cellular energy stress, offering a framework for optimizing drug selection and combination strategies in senescence-targeted interventions.

Wiley Aging CellFeb 12, 2026

Secretome Profiling of Young Multipotent Stem Cells Reveals Angiogenic and Immunomodulatory Mechanisms Supporting Aged Neuromuscular Health

Young muscle-derived stem cells secrete pro-angiogenic and immunomodulatory proteins that decline with age. Systemic transplantation of these young cells into aged mice restored neuromuscular structure and function through paracrine signaling, with effects sustained for two months.

LifeSpan.ioApr 2, 2026

How an Enzyme’s Depletion Makes Fat Worse

Pck1 enzyme depletion in adipose tissue accelerates cellular senescence and metabolic dysfunction, linking metabolic enzyme loss to accelerated aging in fat cells. This identifies a specific enzymatic mechanism by which declining metabolic capacity in aging tissue drives the accumulation of senescent cells and their inflammatory consequences.

Longevity.TechnologyFeb 6, 2026

Rapamycin and the quiet work of immune repair

Low-dose rapamycin protects DNA in aging immune cells by reducing damage-induced cell death and senescence markers, suggesting mTOR inhibition preserves immune resilience through direct genoprotection rather than broad immunosuppression. This mechanistic clarity offers a more tractable regulatory and therapeutic pathway than the traditional anti-aging framing.

Wiley Aging CellApr 14, 2026

Acid–Base Dysregulation Links Aging Metabolism to Frailty

Chronic acid accumulation from aging and stress depletes the body's buffering capacity, disrupting communication between physiological systems and driving frailty through impaired energy metabolism. This acid-base dysregulation mechanism unifies existing frailty models and identifies diet, exercise, and buffering strategies as therapeutic targets.

LifeSpan.ioApr 1, 2026

Rejuvenation Roundup March 2026

This roundup summarizes March 2026 longevity research across multiple domains: mechanisms linking energy production to neurodegeneration, exercise's effect on brain aging, immunosenescence factors, organ-level aging processes, and the interconnection between microbiome composition, psychological state, and systemic aging. The findings collectively advance understanding of how interventions—from resistance training to nutritional composition to social environment—modulate the rate of age-related decline.

Wiley Aging CellApr 21, 2026

UNC45B Reduction With Aging: A Myofiber‐Intrinsic Promoting Factor for Sarcopenia

UNC45B, a myosin chaperone protein, declines with age and is required to maintain fast-twitch muscle force and mass. Loss of UNC45B in skeletal muscle triggers a cascade of systemic effects: reduced contractile capacity precedes atrophy, followed by bone fragility, lower body temperature, and sleep disruption.

Wiley Aging CellMar 9, 2026

Correction to “An Ad Libitum‐Fed Diet That Matches the Beneficial Lifespan Effects of Caloric Restriction but Acts via Opposite Effects on the Energy‐Splicing Axis”

A correction to a study examining how ad libitum feeding can extend lifespan through mechanisms opposite to caloric restriction, particularly involving energy-splicing pathways. This finding challenges the assumption that caloric restriction is the only dietary approach to lifespan extension and suggests multiple metabolic routes can achieve similar longevity outcomes.

LifeSpan.ioFeb 27, 2026

Cellular Reprogramming: The Expert Roundup

Cellular reprogramming—the process of resetting aged cells to younger functional states through partial application of reprogramming factors—represents a fundamental shift in how aging is understood: not as irreversible damage accumulation, but as a modifiable biological state. Clinical trials are imminent, and the field has moved from theoretical elegance to therapeutic platform with potential applications across age-associated diseases.

Wiley Aging CellApr 16, 2026

Ghrelin Receptor Deletion or Pharmacological Inhibition Improves Muscle Function in Aging Male Mice

Blocking the ghrelin receptor improves muscle endurance and mitochondrial function in aging mice without affecting muscle mass or lifespan. Both genetic deletion and pharmacological inhibition restore markers of mitochondrial renewal, suggesting this pathway is a viable therapeutic target for age-related muscle decline.

Wiley Aging CellMar 19, 2026

Aging Triggers an Intestinal Energy Crisis and HDL3 Deficiency Disrupting Gut–Liver Axis Homeostasis

Aging impairs intestinal mitochondrial energy production, reducing HDL3 synthesis and disrupting the gut-liver axis, allowing inflammatory lipopolysaccharide to damage the liver. NMN restores NAD+ availability, rebuilds HDL3 production, and reverses this age-related hepatic injury in experimental models.

SAGE Research on AgingMay 21, 2026

Ageist Language Reduces Health Compliance and Longevity

Research over the past decade reveals ageism embedded in language patterns across healthcare, media, and social contexts—a finding that directly shapes how patients interpret health messaging and comply with medical guidance. The way aging is linguistically framed influences both psychological resilience and health behavior, making communication precision a measurable longevity factor.

Longevity.TechnologyFeb 26, 2026

$30.8m funds Cambrian Bio’s bid to preserve resilience in aging

Cambrian Bio received $30.8 million in ARPA-H funding to test whether a selective mTORC1 inhibitor can preserve intrinsic capacity—the physical and metabolic resilience that maintains function during aging—before disease manifests. This represents a fundamental shift from treating established disease to intervening in the aging process itself, with success measured through a composite biomarker framework rather than disease endpoints.

LifeSpan.ioFeb 23, 2026

How a Sirtuin Protects Against Brain Diseases

SIRT6, a sirtuin protein, protects against neurodegenerative diseases by maintaining nucleolar function and constraining protein synthesis, preventing the accumulation of misfolded proteins that drives age-related brain pathology. This mechanism represents a direct intervention point in proteostasis failure, a primary driver of cognitive decline.

Wiley Aging CellMar 5, 2026

The Immune Cell Atlas of “Longevity Molecular Tag”: Identification of Principal Immune Cell Subsets and Their Underlying Molecular Regulatory Mechanisms

Centenarians maintain immune homeostasis through selective enhancement of cytotoxic immune cells (NK cells, CD8+ T cells, γδ T cells) paired with suppression of inflammatory pathways in adaptive immune populations. This remodeling of immune composition represents a compensatory adaptation mechanism that extends health span and informs potential interventions against immunosenescence.

Wiley Aging CellApr 22, 2026

Multi‐Omics Reveals Mechanisms of Metabolic Rejuvenation in Aged Mice and Pre‐Frail Older Men by Losartan

Losartan, an angiotensin II receptor blocker, partially reversed aging-related metabolomic signatures in both aged mice and pre-frail older men, with effects dependent on functional angiotensin II receptors and correlating with improved survival in treated mice. The drug produced dose-dependent metabolic rejuvenation in humans and normalized age-related shifts in circulating metabolites, particularly lipids and amino acids.

Longevity.TechnologyFeb 6, 2026

Telomir Pharmaceuticals reports new data on epigenetic modulation mechanism

Telomir-1 (Telomir-Zn) modulates intracellular metal balance by increasing zinc and reducing iron, influencing epigenetic regulation and cellular stability without triggering cytotoxic stress. This mechanism addresses oxidative stress and genomic integrity pathways implicated in aging and cancer biology.

Wiley Aging CellFeb 18, 2026

SIRT6 Regulates Protein Synthesis and Folding Through Nucleolar Remodeling

SIRT6 maintains proteostasis by suppressing ribosomal gene expression and translation rates through nucleolar control. Without functional SIRT6, excessive protein synthesis overwhelms the folding machinery, leading to protein aggregation and accelerated neurodegeneration in aging models.

LifeSpan.ioFeb 9, 2026

Restoring the Strength of Natural Killer Cells

Natural killer cells from older adults show reduced capacity to eliminate senescent and cancer cells due to impaired granule release and cytotoxic machinery, not recognition defects. Targeting elevated Cdc42 protein and restoring microtubular organization represents a potential intervention to restore NK cell function with age.

Wiley Aging CellMay 11, 2026

Exosome‐Delivered eNAMPT From Exercise Activates SIRT1 to Counteract Age‐Related Hepatic Steatosis and Fibrosis

Exercise triggers release of exosome-delivered eNAMPT, which activates hepatic SIRT1 and autophagy to reverse age-related fatty liver disease, inflammation, and fibrosis in aged mice. This mechanism establishes a biochemical pathway through which physical activity protects metabolic health during aging.

LT WireMar 11, 2026

Allosteric Bioscience targets longevity research using AI and quantum computing

Allosteric Bioscience is using AI and quantum computing to model molecular mechanisms of aging, targeting pathways including Lamin A, tryptophan metabolism, DNA repair, and mitochondrial function. The approach aims to identify modulators that could reduce age-related disease and extend lifespan.

Biological EDGE

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