+1 Recommend
0 collections
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Bioactive Molecules for Skin Repair and Regeneration: Progress and Perspectives

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          Skin regeneration is a vexing problem in the field of regenerative medicine. A bioactive molecule-based strategy has been frequently used in skin wound healing in recent years. Bioactive molecules are practical tools for regulating cellular processes and have been applied to control cellular differentiation, dedifferentiation, and reprogramming. In this review, we focus on recent progress in the use of bioactive molecules in skin regenerative medicine, by which desired cell types can be generated in vitro for cell therapy and conventional therapeutics can be developed to repair and regenerate skin in vivo through activation of the endogenous repairing potential. We further prospect that the bioactive molecule-base method might be one of the promising strategies to achieve in situ skin regeneration in the future.

          Related collections

          Most cited references 106

          • Record: found
          • Abstract: found
          • Article: found
          Is Open Access

          Fibroblasts and myofibroblasts in wound healing

          (Myo)fibroblasts are key players for maintaining skin homeostasis and for orchestrating physiological tissue repair. (Myo)fibroblasts are embedded in a sophisticated extracellular matrix (ECM) that they secrete, and a complex and interactive dialogue exists between (myo)fibroblasts and their microenvironment. In addition to the secretion of the ECM, (myo)fibroblasts, by secreting matrix metalloproteinases and tissue inhibitors of metalloproteinases, are able to remodel this ECM. (Myo)fibroblasts and their microenvironment form an evolving network during tissue repair, with reciprocal actions leading to cell differentiation, proliferation, quiescence, or apoptosis, and actions on growth factor bioavailability by binding, sequestration, and activation. In addition, the (myo)fibroblast phenotype is regulated by mechanical stresses to which they are subjected and thus by mechanical signaling. In pathological situations (excessive scarring or fibrosis), or during aging, this dialogue between the (myo)fibroblasts and their microenvironment may be altered or disrupted, leading to repair defects or to injuries with damaged and/or cosmetic skin alterations such as wrinkle development. The intimate dialogue between the (myo)fibroblasts and their microenvironment therefore represents a fascinating domain that must be better understood in order not only to characterize new therapeutic targets and drugs able to prevent or treat pathological developments but also to interfere with skin alterations observed during normal aging or premature aging induced by a deleterious environment.
            • Record: found
            • Abstract: found
            • Article: not found

            Expansion and maintenance of human embryonic stem cell-derived endothelial cells by TGFbeta inhibition is Id1 dependent.

            Previous efforts to differentiate human embryonic stem cells (hESCs) into endothelial cells have not achieved sustained expansion and stability of vascular cells. To define vasculogenic developmental pathways and enhance differentiation, we used an endothelial cell-specific VE-cadherin promoter driving green fluorescent protein (GFP) (hVPr-GFP) to screen for factors that promote vascular commitment. In phase 1 of our method, inhibition of transforming growth factor (TGF)beta at day 7 of differentiation increases hVPr-GFP(+) cells by tenfold. In phase 2, TGFbeta inhibition maintains the proliferation and vascular identity of purified endothelial cells, resulting in a net 36-fold expansion of endothelial cells in homogenous monolayers, which exhibited a transcriptional profile of Id1(high)VEGFR2(high)VE-cadherin(+) ephrinB2(+). Using an Id1-YFP hESC reporter line, we showed that TGFbeta inhibition sustains Id1 expression in hESC-derived endothelial cells and that Id1 is required for increased proliferation and preservation of endothelial cell commitment. Our approach provides a serum-free method for differentiation and long-term maintenance of hESC-derived endothelial cells at a scale relevant to clinical application.
              • Record: found
              • Abstract: found
              • Article: not found

              Cutaneous wound healing: recruiting developmental pathways for regeneration

              Following a skin injury, the damaged tissue is repaired through the coordinated biological actions that constitute the cutaneous healing response. In mammals, repaired skin is not identical to intact uninjured skin, however, and this disparity may be caused by differences in the mechanisms that regulate postnatal cutaneous wound repair compared to embryonic skin development. Improving our understanding of the molecular pathways that are involved in these processes is essential to generate new therapies for wound healing complications. Here we focus on the roles of several key developmental signaling pathways (Wnt/β-catenin, TGF-β, Hedgehog, Notch) in mammalian cutaneous wound repair, and compare this to their function in skin development. We discuss the varying responses to cutaneous injury across the taxa, ranging from complete regeneration to scar tissue formation. Finally, we outline how research into the role of developmental pathways during skin repair has contributed to current wound therapies, and holds potential for the development of more effective treatments.

                Author and article information

                Stem Cells Int
                Stem Cells Int
                Stem Cells International
                31 December 2019
                : 2019
                1Wound Healing and Cell Biology Laboratory, Institute of Basic Medical Science, Chinese PLA General Hospital, Beijing 100853, China
                2Trauma Treatment Center, Central Laboratory, Chinese PLA General Hospital, Hainan Branch, 9 Haitang Bay, Sanya 572014, China
                Author notes

                Academic Editor: Jason S. Meyer

                Copyright © 2019 Deyun Chen et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Funded by: General Hospital of PLA Medical Big Data R&D Project
                Award ID: MBD2018030
                Funded by: National S&T Resource Sharing Service Platform Project of China
                Award ID: YCZYPT[2018]07
                Funded by: Military Logistics Research Key Project
                Award ID: AWS17J005
                Funded by: National Natural Science Foundation of China
                Award ID: 81971841
                Award ID: 81721092
                Award ID: 81830064
                Funded by: National Key Research and Development Plan
                Award ID: 2017YFC1103300
                Award ID: 2017YFC1104701
                Review Article

                Molecular medicine


                Comment on this article