Longevity Science · Visual Reference

Mechanisms of Action

Interactive pathway diagrams tracing the molecular cascades behind key longevity interventions — from receptor binding to cellular outcome.

Activator / Trigger
Inhibitor / Blocker
Pathway Node
Downstream Outcome
Six Core Pathways
The Molecular Landscape of Longevity
m
mTOR Pathway
Mechanistic Target of Rapamycin — master regulator of cell growth, protein synthesis, and autophagy. When inhibited, promotes longevity-associated cellular maintenance.
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Growth Factors (IGF-1) PI3K AKT / PKB mTOR Complex 1 Protein Synthesis (S6K) Cell Growth Autophagy Inhibition ✗ Lipid Synthesis Rapamycin / Metformin Fasting / Caloric Restriction (via AMPK) Amino Acids / Insulin Chronic mTOR activation accelerates aging Inhibition shifts resources from growth to maintenance & repair
Rapamycin Metformin NMN
A
AMPK Pathway
AMP-activated Protein Kinase — the cellular energy sensor. Activated under metabolic stress, it triggers catabolic pathways that promote longevity and metabolic health.
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Low Energy (AMP:ATP ↑) Exercise / Fasting Metformin / Berberine LKB1 Kinase AMPK AMP-Activated Protein Kinase Autophagy (ULK1 activation) Mitochondrial Biogenesis (PGC-1α) Glucose Uptake (GLUT4 translocation) Fatty Acid Oxidation (ACC inhib.) mTOR Inhibition ⊣ Cellular Cleanup Energy Production ↑ Insulin Sensitivity ↑ Fat Metabolism ↑ AMPK acts as a metabolic master switch Shifting the cell from anabolic (growth) to catabolic (repair & energy conservation) programs
Metformin Berberine MOTS-c
S
Sirtuin / NAD+ Pathway
NAD+ fuels sirtuin deacetylases (SIRT1–7), key regulators of DNA repair, mitochondrial function, epigenetic maintenance, and inflammatory response.
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NMN (precursor) Tryptophan (de novo) NR (precursor) CD38 consumes NAD+ (aging ↑) NAD+ Pool Sirtuins SIRT1 · SIRT2 · SIRT3 · SIRT4–7 Resveratrol SIRT1 activator DNA Repair (PARP1, SIRT6) Mitochondrial Function (SIRT3, PGC-1α) Inflammation Reduction (NF-κB suppression) Epigenetic Regulation (Histone deacetylation) Genomic Stability Cellular Energy ↑ Reduced Inflammaging Youthful Gene Expr. NAD+ declines ~50% between ages 40 and 60 Restoring NAD+ reactivates sirtuin-mediated cellular maintenance
NMN Nicotinamide Riboside (NR) Resveratrol
G
GLP-1 Signaling
Glucagon-Like Peptide-1 receptor agonists — regulate insulin secretion, appetite, gastric motility, and emerging neuroprotective and cardiovascular effects.
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Semaglutide / Tirzepatide / Retatrutide GLP-1 Ligand Binding DPP-4 degrades native GLP-1 (t½ ~2min) GLP-1 Receptor G-protein coupled (Gsα) cAMP ↑ PKA / EPAC Activation Insulin Secretion ↑ (glucose-dependent) Appetite Suppression (hypothalamic signaling) Gastric Slowing (delayed emptying) Neuroprotection (BDNF, anti-inflam.) Cardio Benefits (anti-atherosclerotic) GLP-1 agonists resist DPP-4 degradation for sustained activation Benefits extend beyond glycemic control to cardiovascular, neurological, and metabolic health
Semaglutide Tirzepatide Retatrutide
♻
Autophagy
The cellular self-eating mechanism — damaged organelles and misfolded proteins are sequestered, delivered to lysosomes, and recycled into raw building blocks.
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Fasting / CR Rapamycin (mTOR inhib.) Spermidine / Fisetin 1. ULK1 Complex Activation ULK1 · ATG13 · FIP200 · ATG101 2. Beclin-1 / VPS34 Complex Nucleation & PI3P generation 3. Phagophore Isolation membrane forms 4. Autophagosome Sealed vesicle LC3-II conjugation Lysosome 5. Fusion 6. Recycled Components Amino acids, lipids, nucleotides Autophagy declines with age, allowing damaged components to accumulate Restoring autophagic flux is a core strategy in longevity research
Rapamycin Spermidine Fisetin
✦
Senescence & Senolytics
Senescent cells cease dividing but resist apoptosis, secreting inflammatory factors (SASP). Senolytic compounds selectively clear these cells, reducing chronic inflammation.
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THE PROBLEM THE SOLUTION DNA Damage Oxidative Stress Telomere Erosion Senescent Cell Growth arrest (p16/p21) + apoptosis resistance SASP IL-6, IL-8, TNF-α, MMPs, VEGF Chronic Inflammation (Inflammaging) Tissue Fibrosis (ECM degradation) Paracrine Senescence (spreads to neighbors) Senolytics Fisetin, D+Q, Navitoclax Selective Clearance Target BCL-2/BCL-xL anti-apoptotic Reduced Inflammation Tissue Rejuvenation Stem cell niche restoration Physical Function ↑ Healthspan ↑ Reduced Age- Related Disease Senescent cell burden increases exponentially after age 60 Periodic senolytic clearance may reduce the inflammatory load driving age-related disease
Fisetin Dasatinib + Quercetin

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