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Metabolic Pathways

Metabolic Pathways Library

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

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Showing 25–48 of 81

Wiley Aging CellApr 7, 2026

Double‐Pronged NAD Preservation: Delaying Cellular Senescence and Initiating Musculoskeletal Regeneration

A combination of NMN and apigenin preserves NAD+ levels, activating SIRT3 to suppress cellular senescence and promote differentiation of muscle, bone, and cartilage precursor cells. The regimen also modulates the gut microbiota to increase production of phytosphingosine, an anti-aging metabolite, resulting in improved musculoskeletal function and exercise capacity in aged animals.

Wiley Aging CellApr 18, 2026

Additional Cover

NAD+ preservation through dual mechanisms—inhibiting its depletion and enhancing its synthesis—delays cellular senescence while promoting musculoskeletal regeneration. This addresses a central constraint in aging: the body's declining capacity to maintain energy production and tissue repair as NAD+ levels fall with time.

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 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.

Nature AgingApr 13, 2026

Exoproteome of calorie-restricted humans identifies complement deactivation as an immunometabolic checkpoint reducing inflammaging

Caloric restriction reduces circulating C3a, a complement protein that drives inflammaging in aged tissues. This identifies a specific immunometabolic pathway through which moderate energy restriction extends healthspan in humans.

Wiley Aging CellApr 23, 2026

Fasting and Caloric Restriction Activate an ADIOL‐NHR‐91‐Kynurenine Pathway Signaling Axis to Promote Healthspan

Fasting and caloric restriction activate ADIOL, a steroid hormone that signals through estrogen receptor β to reduce kynurenic acid in the nervous system and improve healthspan independent of lifespan extension. This mechanism appears evolutionarily conserved and remains effective even when ADIOL is supplemented late in life.

Longevity.TechnologyApr 29, 2026

Nuchido announced as Catalyst Partner for The Longevity Show

Nuchido addresses NAD+ decline through targeted restoration of the salvage pathway rather than simple precursor replacement, supported by randomized controlled human trials demonstrating improvements in inflammation, glycation, and biological age markers. This systems-biology approach represents a maturation of the NAD+ intervention landscape toward mechanistic rather than marketing-driven solutions.

Wiley Aging CellFeb 7, 2026

Rapamycin Reverses the Hepatic Response to Diet‐Induced Metabolic Stress That Is Amplified by Aging

Aging amplifies the liver's inflammatory and metabolic response to high-fat diet, increasing hepatic steatosis and transcriptional dysregulation. Rapamycin treatment reversed most diet-driven gene expression changes in older mice, reducing steatosis, body weight gain, and markers associated with liver disease progression.

LifeSpan.ioApr 9, 2026

A Combination NAD+ Treatment Has Benefits for Mice

Researchers demonstrated that combining NMN supplementation with apigenin—which inhibits NAD+ breakdown—restores muscle function and bone structure in aged mice. This dual approach addresses both supply and preservation of NAD+, a critical coenzyme in cellular energy metabolism and stress resistance.

LifeSpan.ioApr 9, 2026

A Combination NAD+ Treatment Has Benefits for Mice

Researchers demonstrated that combining NAD+ precursor supplementation (NMN) with apigenin, a compound that reduces NAD+ degradation, restores muscle function and bone structure in aged mice. This dual-mechanism approach addresses both NAD+ availability and preservation, with relevance to human aging given prior clinical evidence for NAD+ precursors in metabolic and respiratory function.

Longevity.TechnologyMar 25, 2026

Autophagy angle sharpens Anavex’s investment case for Alzheimer’s

Research published in PNAS Nexus proposes that autophagy dysfunction—a slowdown in cellular recycling—precedes amyloid and tau pathology in Alzheimer's disease. This upstream mechanism shifts the therapeutic target from clearing late-stage debris to restoring the cell's natural cleanup capacity earlier in disease progression.

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.

Wiley Aging CellFeb 15, 2026

Additional Cover

Fasting activates mitochondrial and endothelial repair mechanisms that reverse markers of vascular aging, with implications for extending healthspan through metabolic intervention. The research demonstrates that structured fasting protocols can restore cellular energy production and vascular function independent of weight loss.

LifeSpan.ioApr 21, 2026

Rapamycin Might Blunt Exercise Response in Humans

A randomized, placebo-controlled trial in sedentary adults aged 65-85 found that weekly rapamycin (6 mg) blunted functional gains from a 13-week exercise program, with the placebo group showing greater improvements in chair-stand performance and related measures. The drug's 62-hour half-life likely prevented adequate recovery of mTORC1 signaling between training sessions, creating a pharmacokinetic conflict with exercise adaptation.

Wiley Aging CellMar 31, 2026

Targeting Mitochondrial Stress Responses: Terbinafine and Miglustat as Novel Lifespan and Healthspan Modulators

Terbinafine and miglustat, FDA-approved drugs, extend lifespan and healthspan by inducing mitochondrial stress responses through coordinated activation of ATFS-1 and DAF-16 pathways. This mechanism represents a distinct integration of mitochondrial and insulin signaling stress responses relevant to aging intervention.

Longevity.TechnologyApr 17, 2026

New longevity drug SRN-901 shows 33% lifespan boost

SRN-901, a five-component oral combination therapy, demonstrated a 33% increase in median lifespan and 70% reduction in frailty progression in mice, with preserved physical function and reduced tumor incidence. The multi-pathway approach contrasts with single-target interventions, suggesting that aging requires simultaneous modulation of interconnected biological processes rather than isolated molecular manipulation.

LT WireApr 20, 2026

Seragon study shows SRN-901 extends median lifespan in mice

SRN-901, an oral combinatorial drug, extended median remaining lifespan by 33% in aged mice on a Western diet, with a 46% reduction in hazard of death and 70% attenuation of frailty progression. Multi-omics analysis indicated upregulation of DNA repair and metabolic pathways alongside suppression of inflammatory and oxidative stress responses.

LT WireMar 13, 2026

Renue by Science wins precision recovery & performance award

Renue by Science received recognition for its Total NAD+ Restoration Protocol, a multi-pathway supplement approach designed to address age-related NAD+ decline through enhanced precursor delivery, reduced NAD+ catabolism, improved mitochondrial efficiency, and cellular repair support. NAD+ restoration represents a targeted intervention in the metabolic foundation of cellular aging.

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 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.

Longevity.TechnologyFeb 20, 2026

L-Nutra named Innovator Partner for the Longevity Show 2026

L-Nutra's fasting-mimicking technology platform, validated across 47 clinical trials and 18 university research centers, repositions precision nutrition as essential healthcare infrastructure rather than lifestyle optimization. The company's approach uses targeted nutrient formulations to trigger cellular repair mechanisms—autophagy and metabolic signaling—without the physiological stress of extended fasting, addressing metabolic dysfunction and age-related chronic disease at a systems level.

Longevity.TechnologyMar 18, 2026

Three drugs in major study to prove their capacity to slow aging

UT Health San Antonio is launching VITAL-H, a $38 million clinical trial enrolling over 700 adults to test whether three existing drugs—rapamycin, semaglutide, and dapagliflozin—can slow biological aging in humans. This represents the first large-scale human trial specifically designed to evaluate pharmaceutical intervention in aging processes.

Nature - npj AgingApr 4, 2026

Elevated trimethylamine levels characterize impaired muscle mass response to leucine-enriched protein supplementation in older adults at risk of sarcopenia

Elevated trimethylamine—a gut-derived metabolite—predicts which older adults will fail to gain muscle mass from leucine-enriched protein supplementation. This biomarker distinction reveals that sarcopenia interventions require individual metabolic assessment, not one-size-fits-all protocols.

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.