Matrix metalloproteinase
ProteinMatrix metalloproteinases are zinc‑dependent enzymes that break down extracellular matrix; when chronically upregulated they drive dermal collagen, elastin, and basement‑membrane loss.
44 entities in this category
Matrix metalloproteinases are zinc‑dependent enzymes that break down extracellular matrix; when chronically upregulated they drive dermal collagen, elastin, and basement‑membrane loss.
A 36-amino acid neuropeptide functioning as the brain's fastest and most potent orexigenic signal, a sympathetic co-transmitter in the periphery, and a pro-regenerative modulator in skin.
The master transcription factor coordinating skin inflammation. NF-κB activation simultaneously suppresses barrier proteins and upregulates collagen-degrading MMPs.
The energy-dependent transmembrane transporter that actively pumps protons (H⁺) out of keratinocytes into the stratum corneum extracellular space.
Nuclear receptor and lipid sensor coordinating ceramide, free fatty acid, and cholesterol synthesis simultaneously in keratinocytes.
A single polypeptide precursor that, depending on which tissue processes it, yields entirely different biological outcomes: appetite suppression, cortisol production, photoprotective pigmentation.
A protease‑activated GPCR that guides normal barrier repair under controlled activation but amplifies inflammation, itch, and Th2 signalling when protease activity is dysregulated.
The mitochondrial enzyme that converts pyruvate to acetyl‑CoA and is inhibited by PDK‑mediated phosphorylation, gating glucose entry into oxidative metabolism.
The rate-limiting enzyme initiating de novo ceramide synthesis from serine and palmitoyl-CoA. SPT activity is directly suppressed by declining oestrogen and cortisol elevation.
Liver-produced glycoprotein that binds testosterone, DHT, and oestradiol with high affinity, functioning as the primary gatekeeper of sex hormone bioavailability.
NAD⁺-dependent deacetylase enzymes found in every skin cell. SIRT1 is the most skin-relevant family member, regulating circadian clock amplitude, suppressing NF-κB-driven inflammation.
A keratinocyte‑derived alarmin that translates barrier disruption into Th2 immune activation, driving itch, mast‑cell priming, and the atopic inflammatory cascade.
TGF-β is a pleiotropic cytokine and the master regulator of wound healing, fibrosis, and extracellular matrix remodelling in skin.
TNF is a pro-inflammatory cytokine produced by macrophages, adipocytes, and T-cells that acts through NF-κB to amplify and sustain inflammatory signalling.