BIOEDGE

Biological EDGE

Buy Now

“Meticulous research. Penetrating analysis. A solid framework for change.”  — Dr. Michael J. Krentz

Biological EDGE

Biohacking Starts With NO

Buy Now

“I used to override my body. Now I listen. The difference is stunning.”— Michael Broder

Biohacking Starts With NO
Metabolic Pathways

Metabolic Pathways Library

Every article, presentation, spotlight, and news item we've tagged to Metabolic Pathways.

AllLibraryArticlesPresentationsSpotlightsNews

Showing 49–72 of 79

Wiley Aging CellMay 2, 2026

SIRT1 Downregulation by Advanced Glycation End Products Activates RANKL‐Dependent Osteoclast Signaling and Drives Chondrocyte Senescence During Osteoarthritis Development

Advanced glycation end products suppress SIRT1 expression in osteoclasts, triggering RANKL-dependent bone resorption and accelerated chondrocyte senescence—a mechanism that directly couples metabolic stress to cartilage degradation in osteoarthritis. This pathway represents a biochemical link between systemic glucose metabolism and joint degeneration, suggesting that metabolic control earlier in life may alter osteoarthritis trajectory.

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 AgingMar 31, 2026

Multiomic single-cell perturbation screens reveal critical lncRNA regulators of senescence

A systematic screen of 32 aging-associated long non-coding RNAs identified HOTAIRM1 as a critical regulator of DNA repair pathways, with restoration of HOTAIRM1 in aged mouse lungs reducing fibrosis. This work establishes lncRNA regulation as a targetable mechanism in cellular senescence.

Wiley Aging CellMay 11, 2026

FAM162A Is a Key Regulator of Mitochondrial Structure, Dynamics, and Bioenergetics, Driving Cellular Protection and Longevity

FAM162A, a mitochondrial cristae protein, regulates mitochondrial structure and energy production through interaction with OPA1, enhancing cellular stress resistance and extending lifespan in model organisms. This identifies a previously unrecognized mechanism linking mitochondrial dynamics to organismal longevity.

Nature - npj AgingFeb 18, 2026

Molecular insight into transcriptome profiling of aerobic exercise induced changes in aged skeletal muscle

Aerobic exercise induces measurable transcriptome changes in aged skeletal muscle, activating pathways associated with mitochondrial function, protein synthesis, and cellular stress resilience. These molecular shifts provide a mechanistic explanation for how structured movement preserves muscle quality and metabolic capacity across the lifespan.

Longevity.TechnologyApr 10, 2026

Mitrix moves mitochondria into the clinic

Mitrix Bio has reported preliminary Phase 1 safety data from mitochondrial transplantation in two older adults with no observed adverse effects, while simultaneously launching clinics offering the intervention under Right to Try frameworks. This represents a transition from preclinical work to early clinical deployment, though data density remains limited relative to narrative momentum.

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.

Wiley Aging CellMay 9, 2026

Exceptional Longevity Modifying Allele APOE2 Promotes DNA Signaling Pathways Resisting Cellular Senescence in Human Neurons

APOE2, a genetic variant associated with exceptional longevity, activates DNA repair pathways and resists cellular senescence in neurons, while APOE4 exhibits elevated DNA damage and senescence markers. This mechanism extends beyond lipid metabolism, explaining APOE2's protective effects against neurodegeneration.

Wiley Aging CellApr 25, 2026

Inferring Gene Regulatory Network Architecture Underlying Complex Traits: An Integrative Analysis of Mutant Lifespan and Gene Expression Profiles Identifies Master Regulators and Key Functional Modules for Yeast Aging

Researchers identified a hierarchical gene regulatory network controlling yeast lifespan, where peripheral genes act through master regulators that converge on functional modules governing stress response, autophagy, and proteostasis. This architecture provides a framework for dissecting genetic complexity in aging and maps directly to mechanisms that influence human longevity pathways.

Wiley Aging CellFeb 26, 2026

Lactose‐Derived Carbohydrates Induce Sexually Dimorphic Nutritional Programming Effects on Lifespan in Drosophila melanogaster

Early-life consumption of galactose and glucose (lactose components) extends lifespan in female flies exposed to obesogenic diets in adulthood through reprogramming of lipid metabolism, while reducing lifespan in males. This nutritional programming effect demonstrates that early dietary composition establishes metabolic resilience patterns that persist throughout life and respond differentially by sex.

Wiley Aging CellMar 8, 2026

Aged Male Mice Remain Glucose Tolerant Despite Increased Energy Storage Efficiency Favoring Diet‐Induced Obesity

Aged male mice maintain glucose tolerance despite accumulating more fat on a high-fat diet than younger counterparts, a metabolic uncoupling driven by increased energy storage efficiency and reduced lipid turnover. This finding indicates that obesity and glucose dysregulation diverge with age, presenting distinct intervention targets for metabolic health in older populations.

Nature - npj AgingApr 27, 2026

D-pinitol extends the lifespan of Caenorhabditis elegans through integrated antioxidant defense, proteostasis, and autophagy signaling

D-pinitol, a naturally occurring inositol derivative, extends lifespan in C. elegans by coordinating three distinct cellular mechanisms: antioxidant defense, protein stability (proteostasis), and autophagy. This multi-pathway activation suggests a compound that addresses fundamental aging processes rather than targeting a single intervention point.

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 CellApr 22, 2026

The Mitochondrial NAD Transporter SLC25A51 in Adipocytes Regulates Adipose Tissue Mitochondrial Function and Systemic Metabolism During Aging

SLC25A51, a mitochondrial NAD transporter in fat cells, declines with age and directly regulates adipose tissue energy metabolism and systemic insulin sensitivity. Loss of this transporter accelerates metabolic disease phenotypes; its restoration protects against obesity and insulin resistance in aging.

LT WireMar 14, 2026

Pretzel Therapeutics presents PX578 data supporting POLG disease treatment

PX578, a first-in-class small molecule activator of mitochondrial DNA polymerase gamma, demonstrated preclinical efficacy in restoring mitochondrial DNA levels and cellular energy production across multiple POLG disease models. The compound addresses the underlying genetic defect in mitochondrial DNA depletion syndromes, for which no disease-modifying treatments currently exist.

Longevity.TechnologyMar 26, 2026

Pulmatrix and Eos merge to advance gerotherapeutics

Pulmatrix and Eos SENOLYTIX are merging to develop PTC-2105, a candidate designed to modulate mitochondrial function and clear senescent cells in sarcopenia and metabolic disease. The transaction signals a fundamental shift in biopharma toward targeting aging biology directly rather than its downstream manifestations.

Nature AgingMar 6, 2026

The glycolytic metabolite phosphoenolpyruvate restricts cGAS-driven inflammation to promote healthy aging

Phosphoenolpyruvate, a glycolytic metabolite, suppresses cGAS-STING-driven inflammation and improves cognitive function in Alzheimer's disease models while correlating with healthy aging markers in humans. This identifies a metabolic checkpoint that regulates innate immune signaling during aging.

Wiley Aging CellFeb 13, 2026

Adipose‐Specific GHR Deletion Attenuates Brain Aging and Cognitive Decline in Aged Mice

Blocking growth hormone signaling specifically in adipose tissue reduces neuroinflammation, preserves synaptic integrity, and improves cognitive performance across multiple domains in aged mice. This identifies peripheral adipose tissue as an unexpected regulator of brain aging, suggesting a therapeutic target for age-related cognitive decline.

Wiley Aging CellFeb 25, 2026

Select Small Non‐Coding RNAs Are Determinants of Survival in Older Adults

Circulating small RNAs, particularly nine piRNAs, predict two-year survival in older adults with greater accuracy than age and clinical factors alone, with experimental evidence suggesting reduced piRNA levels associate with extended lifespan. These findings identify specific small RNA signatures as measurable biomarkers and potential therapeutic targets for longevity interventions.

LifeSpan.ioMar 30, 2026

How a Growth Factor and SIRT1 Might Combat Disc Degeneration

FGF21, a growth factor that declines with age, delays intervertebral disc degeneration by upregulating SIRT1 and restoring mitochondrial quality control through the PINK1-Parkin mitophagy pathway. This mechanism addresses a primary driver of age-related lower back pain by counteracting cellular senescence in disc tissue.

Longevity.TechnologyFeb 10, 2026

CagriSema and retatrutide signal the next GLP-1 arms race

Triple and dual agonist drugs like retatrutide and CagriSema target multiple metabolic pathways simultaneously, producing weight loss exceeding 20-30% in clinical trials. These medications represent a shift toward precision metabolic intervention, with implications for both obesity management and aging-related cellular stress.

LifeSpan.ioMar 27, 2026

Mitochondria Delivery Method Rescues Parkinson’s in Mice

Researchers encapsulated healthy mitochondria in red blood cell membranes to deliver them into diseased cells, achieving efficient uptake and functional restoration across multiple cellular models of mitochondrial dysfunction. This addresses a long-standing barrier in mitochondrial replacement therapy and demonstrates potential for treating mitochondrial diseases and age-related energy decline.

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 CellMar 20, 2026

FGF21‐Mediated Upregulation of SIRT1 Delays Intervertebral Disc Degeneration by Promoting PINK1/Parkin Dependent Mitophagy Through Deacetylation of FOXO3

FGF21 activates a cellular repair pathway in spinal disc cells by upregulating SIRT1, which deacetylates FOXO3 and triggers mitochondrial autophagy, thereby suppressing cell senescence and slowing intervertebral disc degeneration. This identifies a targetable molecular axis with direct relevance to preventing age-related spinal structural decline and associated disability.