I cannot answer specifics of your question but this seems along the lines of what you're talking about...
https://journals.physiology.org/doi/full/10.1152/japplphysiol.00945.2010
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BPC 157 promoted the ex vivo outgrowth of tendon explants.
To clarify the potential mechanism of BPC 157 on promoting tendon healing, the initial outgrowth of tendon fibroblasts from tendon explants cultured with or without 2 μg/ml BPC 157 was examined and compared. At the 2nd day after implantation, tendon fibroblasts migrating out from the tendon explant were observed in 5 of 10 tendon explants in the BPC 157 group compared with 2 of 10 tendon explants in the control group. At the 5th day, the outgrowth of tendon fibroblasts was observed in all the tendon explants in two groups. This result indicated that BPC 157 could accelerate cell outgrowth from the tendon explant. In addition, the total number of tendon fibroblasts outgrowth from the explants after 7 days of incubation was significantly increased in the BPC 157 group (
Fig. 1B). Representative pictures from the two groups are shown in
Fig. 1A.
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Healing of the injured tendon involves a lot of complex pathways. It progresses through overlapping stages of inflammation, regeneration, and remodeling. The whole process is slow, and the strength of the healed tendon is inadequate. It heals by scars, which take at least 1 year for maturation. The scar tissue has reduced mechanical strength and renders the tendon susceptible to reinjury (
16). This process of regeneration is believed to occur either extrinsically by infiltration of external cells or intrinsically by tendon fibroblast proliferation or both. Migration and proliferation of cells seem to be fundamental for tendon healing.
The beneficial effect of BPC 157 was confirmed by the acceleration of initial outgrowth of tendon fibroblasts from tendon explant. This experiment was designed to mimic the very early stage of tendon regeneration, during which period tendon fibroblasts migrate from either epitendon or endotendon (
9,
20). This influence was also confirmed by the transwell filter migration experiments. Tendon cells with 24 h treatment with BPC 157 significantly increases their migratory speed up to 2.3-fold at the concentration of 2 μg/ml.
In our experiments, BPC 157 had no direct effect on promoting the proliferation of an in vitro culture of tendon fibroblasts, which could also be verified by the unaltered expression of PCNA protein after 24 h of treatment with BPC 157. Since cell proliferation is an important process of tendon healing, the result was unexpected. However, we understood that the experimental condition using in vitro culture of tendon fibroblasts could not mimic the real environment of tendon. During the course of in vivo healing, other cells such as leukocytes and stem cells may also interact with each other and contribute to this complicated process. It is possible that the healing-accelerating effect of BPC 157 may act on other cells and exert an indirect effect on promoting the proliferation of tendon fibroblasts. An additional explanation is that the effect of BPC 157 has been shown to be restricted to diseased conditions, and therefore the proliferation of normal tendon fibroblasts is not affected. In a study carried out by Staresinic et al. (
29), the proliferation-enhanced activity of BPC 157 was only demonstrated in HNE-damaged cells but not in normal cells. We also demonstrated that BPC 157 could increase the cell survival of tendon fibroblasts under the oxidative stress of H2O2. However, the underlying protective mechanism of BPC 157 needs to be further investigated.
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This is the first report to show that the healing effect of BPC 157 could be mediated by activating a cellular FAK-paxillin signal pathway. However, it is still mysterious how exactly BPC 157 generates the integrin-stimulated signals and consequently activates the downstream FAK. Whether BPC 157 can act as a ligand to bind directly to a membrane receptor will be of great interest to study in the future.
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Also GHK-cu has been shown to help with eliminating scar tissue however I am unsure if it's limited to only certain tissues or if it applies to tendons as well. I have used it in conjunction with BPC/TB
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6073405/
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In the past, the wound healing, tissue remodeling, angiogenesis-promoting, cell-growth stimulating, anti-inflammatory and anti-oxidant actions of GHK were attributed to its unique relationship with copper. Copper is a transitional metal that is vital for all eukaryotic organisms from microbes to humans. Since it can be converted from oxidized Cu(II) to reduced Cu(I) form, it functions as an essential co-factor in a multitude of biochemical reactions involving electron transfer. A dozen enzymes (cuproenzymes) use changes in copper oxidation states to catalyze important biochemical reactions, including cellular respiration (cytochrome c oxidase), antioxidant defense (ceruloplasmin, superoxide dismutase (SOD), detoxification (metallothioneins), blood clotting (blood clotting factors V and VIII), and the connective tissue formation (lysyl peroxidase). Copper is required for iron metabolism, oxygenation, neurotransmission, embryonic development and many other essential biological processes [
64]."
https://www.peptidesciences.com/blog/what-is-ghk-cu-and-how
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Mechanism of Action
GHK-Cu exerts its action on a variety of pathways in the human body due to the peptide sequence and copper’s ability to promote various functions. At the site of tissue injury, GHK-Cu acts as a potent chemoattractant for mast cells, macrophages, amongst others which promote the release of proteins that stimulate the growth and repair of tissue. As stated before, GHK-Cu acts in a dual manner to remove scar tissue from injured locations and replace it with new tissue. Primarily, it acts directly on fibroblasts by increasing production of mRNA and protein for collagen, elastin, proteoglycans, glycosaminoglycans, and decorin; all of which are critical components in tissue repair and maintenance. Further, it acts to stimulate the production of metalloproteases and protease inhibitors which function to remove damaged tissue proteins. It also reduced the secretion of TGF-beta from fibroblasts during this process as TGF-beta acts to induce scar formation."
