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ABSTRACT
Introduction
Understanding the molecular and cellular processes involved in skin wound healing may pave the way for the development of innovative approaches to transforming the identified natural effectors into therapeutic tools. Based on the extensive involvement of the ga(lactoside-binding)lectin family in (patho)physiological processes, it has been well established that galectins are involved in a wide range of cell-cell and cell-matrix interactions.
Areas covered
In the present paper, we provide an overview of the biological role of galectins in repair and regeneration, focusing on four main phases (hemostasis, inflammation, proliferation, and maturation/remodeling) of skin repair using basic wound models (open excision vs. sutured incision).
Expert opinion
The reported data make a strong case for directing further efforts to treat excisional and incisional wounds differently. Functions of galectins essentially result from their modular presentation. In fact, Gal-1 seems to play a role in the early phases of healing (anti-inflammatory) and wound contraction, Gal-3 accelerates re-epithelization and increases tensile strength (scar inductor). Galectins have also become subject of redesigning by engineering to optimize the activity. Clinically relevant, these new tools derived from the carbohydrate recognition domain platform may also prove helpful for other purposes, such as potent antibacterial agglutinins and opsonins.
Article highlights
Galectins (type and dose dependent) fine tune immune responses affecting the healing outcome.
Galectin-1 activates SMAD pathway leading to improved contraction of open wounds.
Galectin-3 favorably increases wound tensile strength of healing skin incisions.
Galectin-3 improves epidermis regeneration and collagen maturation in both open and sutured wounds.
Reported data make a strong case for directing further efforts to treat excisional and incisional wounds differently.
This box summarizes key points contained in the article.
Declaration of interest
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.
Paper dedication
This paper is dedicated to the memory of our dear colleague and friend Hans-Joachim Gabius. Professor Hans-Joachim Gabius passed away unexpectedly on Monday, 2 August 2021. He died shortly before his retirement, which would have been on 30 September 2021. His death leaves us in sadness and grief. It was a privilege to work with him scientifically, and we are grateful for his inspiration and daily motivation. We are very proud of the papers we published with him and the opportunity to develop the concept of the sugar code together. His death is a tremendous loss for the field of glycobiology/chemistry.
Professor Hans-Joachim Gabius was the founder and pillar of the concept of the sugar code. He published over 800 scientific papers that were cited more than 30,000 times (H-index = 90). He was granted many distinguished awards. Professor Gabius served as the editorial board member of several international journals, including Expert Opinion on Therapeutic Targets. Professor Gabius inspired and motivated us with brilliant new ideas throughout his scientific carrier.
Supplementary material
Supplemental data for this article can be accessed online at https://doi.org/10.1080/14728222.2023.2175318