Advertisement
Invited Review Article| Volume 76, ISSUE 3, P169-172, December 2014

Attempts to accelerate wound healing

Published:November 11, 2014DOI:https://doi.org/10.1016/j.jdermsci.2014.11.001

      Abstract

      Wound healing is a well-orchestrated process, where numerous factors are activated or inhibited in a sequence of steps. Immediately after the infliction of damage, the repair of wound stars. The initial step is an inflammatory change with activation of innate immunity, which is followed by proliferation phase, including fibroplasia, angiogenesis and re-epithelialization. Pathological impairment of wound healing process may lead to persistent ulceration as seen in diabetic patients. Various signaling pathways are involved in wound healing. TGFβ/Smad pathway is a representative and well known to participate in fibroplasia, however, its comprehensive effect on wound healing is controversial. Experimental and clinical remedies have been being tried to promote wound healing. Advancement of cell engineering allows us to use stem cells and living skin equivalents.

      Keywords

      To read this article in full you will need to make a payment

      Purchase one-time access:

      Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
      One-time access price info
      • For academic or personal research use, select 'Academic and Personal'
      • For corporate R&D use, select 'Corporate R&D Professionals'

      Subscribe:

      Subscribe to Journal of Dermatological Science
      Already a print subscriber? Claim online access
      Already an online subscriber? Sign in
      Institutional Access: Sign in to ScienceDirect

      References

        • Lamkanfi M.
        Emerging inflammasome effector mechanisms.
        Nat Rev Immunol. 2011; 11: 213-220
        • Hirsiger S.
        • Simmen H.P.
        • Werner C.M.
        • Wanner G.A.
        • Rittirsch D.
        Danger signals activating the immune response after trauma.
        Mediat Inflamm. 2012; 2012: 315941
        • Koh T.J.
        • DiPietro L.A.
        Inflammation and wound healing: the role of the macrophage.
        Expert Rev Mol Med. 2011; 13: e23
        • Brancato S.K.
        • Albina J.E.
        Wound macrophages as key regulators of repair: origin, phenotype, and function.
        Am J Pathol. 2011; 178: 19-25
        • Gallucci R.M.
        • Simeonova P.P.
        • Matheson J.M.
        • Kommineni C.
        • Guriel J.L.
        • Sugawara T.
        • et al.
        Impaired cutaneous wound healing in interleukin-6-deficient and immunosuppressed mice.
        FASEB J. 2000; 14: 2525-2531
        • Mori R.
        • Kondo T.
        • Ohshima T.
        • Ishida Y.
        • Mukaida N.
        Accelerated wound healing in tumor necrosis factor receptor p55-deficient mice with reduced leukocyte infiltration.
        FASEB J. 2002; 16: 963-974
        • Ishida Y.
        • Kondo T.
        • Takayasu T.
        • Iwakura Y.
        • Mukaida N.
        The essential involvement of cross-talk between IFN-gamma and TGF-beta in the skin wound-healing process.
        J Immunol. 2004; 172: 1848-1855
        • Matias M.A.
        • Saunus J.M.
        • Ivanovski S.
        • Walsh L.J.
        • Farah C.S.
        Accelerated wound healing phenotype in interleukin 12/23 deficient mice.
        J Inflamm (Lond). 2011; 8: 39
        • Ishida Y.
        • Kondo T.
        • Kimura A.
        • Matsushima K.
        • Mukaida N.
        Absence of IL-1 receptor antagonist impaired wound healing along with aberrant NF-kappaB activation and a reciprocal suppression of TGF-beta signal pathway.
        J Immunol. 2006; 176: 5598-5606
        • Eming S.A.
        • Werner S.
        • Bugnon P.
        • Wickenhauser C.
        • Siewe L.
        • Utermohlen O.
        • et al.
        Accelerated wound closure in mice deficient for interleukin-10.
        Am J Pathol. 2007; 170: 188-202
        • Suga H.
        • Sugaya M.
        • Fujita H.
        • Asano Y.
        • Tada Y.
        • Kadono T.
        • et al.
        TLR4, rather than TLR2, regulates wound healing through TGF-beta and CCL5 expression.
        J Dermatol Sci. 2014; 73: 117-124
        • Hasegawa M.
        • Higashi K.
        • Matsushita T.
        • Hamaguchi Y.
        • Saito K.
        • Fujimoto M.
        • et al.
        Dermokine inhibits ELR(+)CXC chemokine expression and delays early skin wound healing.
        J Dermatol Sci. 2013; 70: 34-41
        • Greaves N.S.
        • Ashcroft K.J.
        • Baguneid M.
        • Bayat A.
        Current understanding of molecular and cellular mechanisms in fibroplasia and angiogenesis during acute wound healing.
        J Dermatol Sci. 2013; 72: 206-217
        • Samuel G.H.
        • Lenna S.
        • Bujor A.M.
        • Lafyatis R.
        • Trojanowska M.
        Acid sphingomyelinase deficiency contributes to resistance of scleroderma fibroblasts to Fas-mediated apoptosis.
        J Dermatol Sci. 2012; 67: 166-172
        • Canady J.
        • Karrer S.
        • Fleck M.
        • Bosserhoff A.K.
        Fibrosing connective tissue disorders of the skin: molecular similarities and distinctions.
        J Dermatol Sci. 2013; 70: 151-158
        • Ueda-Hayakawa I.
        • Hasegawa M.
        • Hamaguchi Y.
        • Takehara K.
        • Fujimoto M.
        Circulating gamma/delta T cells in systemic sclerosis exhibit activated phenotype and enhance gene expression of proalpha2(I) collagen of fibroblasts.
        J Dermatol Sci. 2013; 69: 54-60
        • Liang M.
        • Lv J.
        • Chu H.
        • Wang J.
        • Chen X.
        • Zhu X.
        • et al.
        Vertical inhibition of PI3K/Akt/mTOR signaling demonstrates in vitro and in vivo anti-fibrotic activity.
        J Dermatol Sci. 2014; 76: 104-111
        • Bellavia G.
        • Fasanaro P.
        • Melchionna R.
        • Capogrossi M.C.
        • Napolitano M.
        Transcriptional control of skin reepithelialization.
        J Dermatol Sci. 2014; 73: 3-9
        • Liu J.
        • Wang Y.
        • Pan Q.
        • Su Y.
        • Zhang Z.
        • Han J.
        • et al.
        Wnt/beta-catenin pathway forms a negative feedback loop during TGF-beta1 induced human normal skin fibroblast-to-myofibroblast transition.
        J Dermatol Sci. 2012; 65: 38-49
        • Lee C.H.
        • Hong C.H.
        • Chen Y.T.
        • Chen Y.C.
        • Shen M.R.
        TGF-beta1 increases cell rigidity by enhancing expression of smooth muscle actin: keloid-derived fibroblasts as a model for cellular mechanics.
        J Dermatol Sci. 2012; 67: 173-180
        • Yamaoka H.
        • Sumiyoshi H.
        • Higashi K.
        • Nakao S.
        • Minakawa K.
        • Sumida K.
        • et al.
        A novel small compound accelerates dermal wound healing by modifying infiltration, proliferation and migration of distinct cellular components in mice.
        J Dermatol Sci. 2014; 74: 204-213
        • Lee M.J.
        • Shin J.O.
        • Jung H.S.
        Thy-1 knockdown retards wound repair in mouse skin.
        J Dermatol Sci. 2013; 69: 95-104
        • Ebaid H.
        • Ahmed O.M.
        • Mahmoud A.M.
        • Ahmed R.R.
        Limiting prolonged inflammation during proliferation and remodeling phases of wound healing in streptozotocin-induced diabetic rats supplemented with camel undenatured whey protein.
        BMC Immunol. 2013; 14: 31
        • Straino S.
        • Di Carlo A.
        • Mangoni A.
        • De Mori R.
        • Guerra L.
        • Maurelli R.
        • et al.
        High-mobility group box 1 protein in human and murine skin: involvement in wound healing.
        J Invest Dermatol. 2008; 128: 1545-1553
        • Rivas-Santiago B.
        • Trujillo V.
        • Montoya A.
        • Gonzalez-Curiel I.
        • Castaneda-Delgado J.
        • Cardenas A.
        • et al.
        Expression of antimicrobial peptides in diabetic foot ulcer.
        J Dermatol Sci. 2012; 65: 19-26
        • Morhenn V.B.
        • Nelson T.E.
        • Gruol D.L.
        The rate of wound healing is increased in psoriasis.
        J Dermatol Sci. 2013; 72: 87-92
        • Kanno E.
        • Kawakami K.
        • Miyairi S.
        • Tanno H.
        • Otomaru H.
        • Hatanaka A.
        • et al.
        Neutrophil-derived tumor necrosis factor-alpha contributes to acute wound healing promoted by N-(3-oxododecanoyl)-l-homoserine lactone from Pseudomonas aeruginosa.
        J Dermatol Sci. 2013; 70: 130-138
        • Bosanquet D.C.
        • Ye L.
        • Harding K.G.
        • Jiang W.G.
        Expressed in high metastatic cells (Ehm2) is a positive regulator of keratinocyte adhesion and motility: the implication for wound healing.
        J Dermatol Sci. 2013; 71: 115-121
        • Cheret J.
        • Lebonvallet N.
        • Buhe V.
        • Carre J.L.
        • Misery L.
        • Le Gall-Ianotto C.
        Influence of sensory neuropeptides on human cutaneous wound healing process.
        J Dermatol Sci. 2014; 74: 193-203
        • Huang S.
        • Lu G.
        • Wu Y.
        • Jirigala E.
        • Xu Y.
        • Ma K.
        • et al.
        Mesenchymal stem cells delivered in a microsphere-based engineered skin contribute to cutaneous wound healing and sweat gland repair.
        J Dermatol Sci. 2012; 66: 29-36
        • Kim H.
        • Choi K.
        • Kweon O.K.
        • Kim W.H.
        Enhanced wound healing effect of canine adipose-derived mesenchymal stem cells with low-level laser therapy in athymic mice.
        J Dermatol Sci. 2012; 68: 149-156
        • Song S.H.
        • Lee M.O.
        • Lee J.S.
        • Jeong H.C.
        • Kim H.G.
        • Kim W.S.
        • et al.
        Genetic modification of human adipose-derived stem cells for promoting wound healing.
        J Dermatol Sci. 2012; 66: 98-107
        • Iwata Y.
        • Akamatsu H.
        • Hasegawa S.
        • Takahashi M.
        • Yagami A.
        • Nakata S.
        • et al.
        The epidermal integrin beta-1 and p75NTR positive cells proliferating and migrating during wound healing produce various growth factors, while the expression of p75NTR is decreased in patients with chronic skin ulcers.
        J Dermatol Sci. 2013; 71: 122-129
        • Renner R.
        • Simon J.C.
        New insights into therapy by mathematical analysis: recalcitrant granulated improved more than sclerotic venous leg ulcers with amelogenin treatment.
        J Dermatol Sci. 2012; 67: 15-19
        • Ananta M.
        • Brown R.A.
        • Mudera V.
        A rapid fabricated living dermal equivalent for skin tissue engineering: an in vivo evaluation in an acute wound model.
        Tissue Eng A. 2012; 18: 353-361
        • Felder 3rd, J.M.
        • Goyal S.S.
        • Attinger C.E.
        A systematic review of skin substitutes for foot ulcers.
        Plast Reconstr Surg. 2012; 130: 145-164
        • Yang L.
        • Hashimoto K.
        • Tohyama M.
        • Okazaki H.
        • Dai X.
        • Hanakawa Y.
        • et al.
        Interactions between myofibroblast differentiation and epidermogenesis in constructing human living skin equivalents.
        J Dermatol Sci. 2012; 65: 50-57
        • Webster J.
        • Scuffham P.
        • Stankiewicz M.
        • Chaboyer W.P.
        Negative pressure wound therapy for skin grafts and surgical wounds healing by primary intention.
        Cochrane Database Syst Rev. 2014; 10: CD009261
        • Hsu C.C.
        • Chow S.E.
        • Chen C.P.
        • Tsai W.C.
        • Wang J.S.
        • Yu S.Y.
        • et al.
        Negative pressure accelerated monolayer keratinocyte healing involves Cdc42 mediated cell podia formation.
        J Dermatol Sci. 2013; 70: 196-203

      Biography

      Akira Kasuya received the MD from Niigata University, Japan, in 2006. He moved to Hamamatsu University School of Medicine. He was assigned as an Assistant Professor at Department of Dermatology in 2011. His interests are wound healing and immunology.