Zaid H. Khoury, Fadi Salameh
2021
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Journal
Regenerative Engineering and Translational Medicine
Abstract
This manuscript reviews the current state of research on the regenerative properties of trodusquemine, a promising naturally occurring compound with the potential to be employed to regenerate skin and mucosal wounds, particularly when the wound healing capacity is diminished. The skin and mucous membranes lining body cavities differ in their intrinsic regenerative potential, which can be further modified by local and systemic biomedical factors that ultimately delay the natural course of wound healing, leading to increased morbidity. Non-receptor type 1 protein tyrosine phosphatase (PTP1B), the target of trodusquemine, was found to be overexpressed in the setting of uncontrolled diabetes mellitus mediating poor wound healing responses. PTP1B inhibition was shown to decrease inflammation and enhance angiogenesis, promoting wound regeneration in the context of diabetes. Trodusquemine has demonstrated phenomenal ability in regenerating various tissues in vivo through the inhibition of PTP1B, eliminating the disruptive dephosphorylation of receptor tyrosine kinases, allowing transmission of tissue regenerative signals to the nucleus, and ultimately the regrowth of damaged tissue. Further evidence in the form of well-controlled in vitro and in vivo studies to evaluate the role of PTP1B in the wound healing cascade is mandated. Trodusquemine-mediated inhibition of PTP1B may potentially revolutionize regenerative medicine and dentistry particularly in the setting of diminished wound healing responses. Trodusquemine is currently the sole small molecule with mammalian tissue regenerative potential that proved to be safely tolerated in humans. Trodusquemine acts through the inhibition of an enzyme, namely, non-receptor type 1 protein tyrosine phosphatase, allowing for tissue regeneration. When the tissue is wounded under most ordinary circumstances, this aforementioned enzyme regulates cellular growth by terminating the signaling pathway responsible for tissue regrowth in an attempt to prevent uncontrolled cellular proliferation at sites of injury, which in turn encourages healing by scar formation.