TGF-β signaling
The superfamily containing the BMPs — and a signal whose effect depends entirely on context.
Transforming growth factor beta names both a specific molecule and the superfamily it heads — a family that includes the bone morphogenetic proteins. Signalling runs through receptor complexes to SMAD proteins, which carry the message to the nucleus. Broadly, BMP ligands signal via SMAD1/5/8, TGF-β proper via SMAD2/3, which is how one family produces divergent outcomes.
TGF-β is the canonical context-dependent signal. It drives matrix production and is essential to repair, yet excessive or prolonged TGF-β activity is a principal driver of fibrosis — the scar outcome the field is trying to avoid. The same molecule builds and over-builds; timing and dose separate the two.
In bone, TGF-β is stored in the mineralised matrix and released during resorption, where it helps couple resorption to formation. It also interacts extensively with Wnt — these pathways are a network, not independent lines.
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