testosterone36
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thread music:
GHK-Cu can influence pathways overlapping with TGF-beta, in fibrosis models it tends to dampen excessive TGF-beta1/SMAD2/3 signaling ,,
TGF-beta is part of normal growth-plate regulation
TGF-beta signaling participates in regulating this sequence alongside BMP, IHH–PTHrP, FGF/FGFR3, Wnt, GH/IGF-1, thyroid hormone, and sex steroids
TGF-beta isoforms are expressed in the perichondrium and epiphyseal growth plate.
TGF-beta2 has an important developmental role in animal skeletal development.
In growth-plate chondrocytes, TGF-beta can slow maturation and restrain terminal hypertrophic differentiation. In principle, that may help preserve orderly cartilage architecture and prevent chondrocytes from moving too quickly into the final hypertrophic, mineralizing, bone-replaced state.
BUT
A theoretically favorable state is not high TGF-beta; it’s an appropriately regulated signal that preserves resting / proliferative chondrocytes and matrix organization while avoiding excessive hypertrophy, premature vascular invasion, and replacement of cartilage by bone. That balance must also remain coordinated with BMP and IHH & PTHrP signaling, which regulate proliferation and differentiation across the plate.
now the best part
GHK-Cu has been reported to reduce abnormally elevated TGF-beta1 & SMAD2/3 activity in experimental pulmonary fibrosis, which is compatible with an antifibrotic action.
****That should be interpreted as modulation of a pathologically activated pathway not evidence that it raises, preserves, or optimizes TGF-beta signaling
in healthy growth-plate cartilage****
but from my understanding
chronically excessive or mislocalized
TGF-beta can be more damaging than mildly low signaling,
so it may be important to REGULATE tgf-b signaling with GHK-Cu
GHK-Cu can influence pathways overlapping with TGF-beta, in fibrosis models it tends to dampen excessive TGF-beta1/SMAD2/3 signaling ,,
TGF-beta is part of normal growth-plate regulation
TGF-beta signaling participates in regulating this sequence alongside BMP, IHH–PTHrP, FGF/FGFR3, Wnt, GH/IGF-1, thyroid hormone, and sex steroids
TGF-beta isoforms are expressed in the perichondrium and epiphyseal growth plate.
TGF-beta2 has an important developmental role in animal skeletal development.
In growth-plate chondrocytes, TGF-beta can slow maturation and restrain terminal hypertrophic differentiation. In principle, that may help preserve orderly cartilage architecture and prevent chondrocytes from moving too quickly into the final hypertrophic, mineralizing, bone-replaced state.
BUT
A theoretically favorable state is not high TGF-beta; it’s an appropriately regulated signal that preserves resting / proliferative chondrocytes and matrix organization while avoiding excessive hypertrophy, premature vascular invasion, and replacement of cartilage by bone. That balance must also remain coordinated with BMP and IHH & PTHrP signaling, which regulate proliferation and differentiation across the plate.
now the best part
GHK-Cu has been reported to reduce abnormally elevated TGF-beta1 & SMAD2/3 activity in experimental pulmonary fibrosis, which is compatible with an antifibrotic action.
****That should be interpreted as modulation of a pathologically activated pathway not evidence that it raises, preserves, or optimizes TGF-beta signaling
in healthy growth-plate cartilage****
but from my understanding
chronically excessive or mislocalized
TGF-beta can be more damaging than mildly low signaling,
so it may be important to REGULATE tgf-b signaling with GHK-Cu
