The science of aging well. Research on NAD+ supplementation, cellular repair, telomere health, mitochondrial function, and anti-aging protocols designed to extend healthspan and optimize long-term vitality.
Matrikines are peptide fragments liberated when collagen and elastin break down — and they act as feedback signals telling fibroblasts to rebuild the extracellular matrix.
Matrix metalloproteinases MMP-1, MMP-2, and MMP-9 are the primary enzymes responsible for collagen destruction in photoaged skin. Understanding their UV-driven upregulation and TIMP-mediated counter-regulation reveals the molecular basis of dermal aging.
NMN faces a pharmacokinetic paradox: it raises NAD+ in tissues even though most oral doses are degraded before absorption. Understanding the Slc12a8 transporter and the NMN-to-NR-to-NMN cycle explains why delivery route fundamentally shapes outcomes.
Decorin is the small leucine-rich proteoglycan that dictates collagen fiber diameter, spacing, and tensile behavior in skin — controlling dermal architecture far more than collagen quantity alone.
Decorin is the unsung architect of dermal collagen — regulating fibril diameter, binding TGF-β, and modulating repair. Its loss with photoaging reframes skin aging as a proteoglycan deficit, not merely collagen depletion.
The Na+/K+-ATPase consumes nearly a third of the body's resting energy budget to maintain the ion gradients that make life possible. Its decline drives neuronal hyperexcitability, arrhythmia, and cognitive aging.
CD38 is the dominant consumer of NAD+ in aging tissues, and its activity rises sharply with inflammaging and senescent cell accumulation — making it a central enzymatic axis linking metabolic decline to cellular aging.
PGC-1α is the transcriptional coactivator that builds mitochondria, enables oxidative metabolism, and powers brown fat thermogenesis. Its age-related decline is a central driver of metabolic inflexibility.
MMP-1 and MMP-9 are zinc-dependent enzymes that UV radiation activates within hours of sun exposure, cleaving type I and type III collagen and accelerating dermal aging. Understanding TIMP regulators and copper peptide modulation reveals why some interventions reverse photoaging while others fail.
Matrikines are peptide fragments liberated from collagen, elastin, and laminin during extracellular matrix turnover. Unlike growth factors, they directly instruct fibroblasts to remodel tissue — making them a foundational target in dermal aging therapy.