Scar-Free Healing: Current Concepts and Future Perspectives

Abstract

Every year, millions of people develop scars due to skin injuries after trauma, surgery, or skin burns. From the beginning of wound healing development, scar hyperplasia, and prolonged healing time in wound healing have been severe problems. Based on the difference between adult and fetal wound healing processes, many promising therapies have been developed to decrease scar formation in skin wounds. Currently, there is no good or reliable therapy to cure or prevent scar formation. This work briefly reviews the engineering methods of scarless wound healing, focusing on regenerative biomaterials and different cytokines, growth factors, and extracellular components in regenerative wound healing to minimize skin damage cell types, and scar formation.

Keywords: regenerative biomaterials; regenerative capacity; scar-free wound regeneration; scarring; skin regeneration; tissue regeneration; wound healing.

Figure 1

Histological image—hematoxylin–eosin stages of the wound healing process (10×, bar: 20 µm) (a) physiological skin, (b) damaged skin, (c) skin undergoing wound healing process and (d) healed skin [19].

Figure 2

Wound healing process and cells involved in each phase: (A) hemostasis, (B) inflammation, (C) proliferation, (D) remodeling [19].

Figure 3

Transforming growth factor β (TGF-β) isoforms and their role in wound healing—schematical representation [54].

Figure 4

Regulators of wound healing and scarring (blue indicates activation, and pink indicates attenuation of fibrosis) [3].

Figure 5

Cutaneous wounds (A) 3 days and (B) 5 days after injury [7].

Figure 6

(a) Various TGF-β signatures; (b) the amount of TGF-β varies in the epidermis through the sequential stages of wound healing [89].

Figure 7

Growth factor-loaded drug delivery systems (DDSs) for enhanced wound healing [7].

Figure 8

Schematically ilustration of hBM-MSC-Ex stimulates cutaneous wound healing by regulating the TGF-β/Smad signal pathway [138].