Autophagy
The cell's recycling process — sequestering and degrading damaged proteins and organelles.
Autophagy ('self-eating') is the cellular process by which damaged or unneeded proteins and organelles are sequestered in autophagosomes and delivered to lysosomes for degradation. It maintains cellular homeostasis, removes mitochondrial damage (mitophagy), and is up-regulated under nutrient stress (fasting). Reduced autophagy is associated in the literature with ageing, neurodegeneration, and metabolic dysfunction; pharmacological enhancement (rapamycin, spermidine) is an active longevity research area. mTOR is the most-studied negative regulator of autophagy.
- GlossarymTOR
Mechanistic target of rapamycin — a master regulator of cell growth, metabolism, and autophagy.
- GlossarySirtuin
A family of NAD+-dependent deacetylase enzymes implicated in longevity and metabolic regulation.
- GlossaryGLP-1
Glucagon-like peptide-1, an incretin hormone that regulates glucose and appetite.
- ResearchMOTS-c 40 mg
MOTS-c is a 16-residue peptide encoded in the mitochondrial 12S rRNA region. Described by the Cohen lab in 2015 — studied in metabolic and exercise bi
- ResearchNAD⁺ 500 mg kit
Nicotinamide adenine dinucleotide — the coenzyme central to cellular electron-transfer, sirtuin signalling, and redox biology.