<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE root>
<article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="review-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">RUDN Journal of Medicine</journal-id><journal-title-group><journal-title xml:lang="en">RUDN Journal of Medicine</journal-title><trans-title-group xml:lang="ru"><trans-title>Вестник Российского университета дружбы народов. Серия: Медицина</trans-title></trans-title-group></journal-title-group><issn publication-format="print">2313-0245</issn><issn publication-format="electronic">2313-0261</issn><publisher><publisher-name xml:lang="en">Peoples’ Friendship University of Russia named after Patrice Lumumba (RUDN University)</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">27540</article-id><article-id pub-id-type="doi">10.22363/2313-0245-2021-25-3-235-242</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>DERMATOLOGY</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>ДЕРМАТОЛОГИЯ</subject></subj-group><subj-group subj-group-type="article-type"><subject>Review Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">Transforming growth factor beta-1 and vascular endothelial growth factor in the recovery and formation of skin scars</article-title><trans-title-group xml:lang="ru"><trans-title>Роль трансформирующего фактор роста бета-1 и фактора роста эндотелия сосудов в формировании кожных рубцов</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-9453-4262</contrib-id><name-alternatives><name xml:lang="en"><surname>Nikonorova</surname><given-names>Varvara G.</given-names></name><name xml:lang="ru"><surname>Никонорова</surname><given-names>В. Г.</given-names></name></name-alternatives><email>bgnikon@gmail.com</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-9267-5800</contrib-id><name-alternatives><name xml:lang="en"><surname>Chrishtop</surname><given-names>Vladimir V.</given-names></name><name xml:lang="ru"><surname>Криштоп</surname><given-names>В. В.</given-names></name></name-alternatives><email>bgnikon@gmail.com</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-8035-4065</contrib-id><name-alternatives><name xml:lang="en"><surname>Rumyantseva</surname><given-names>Tatyana A.</given-names></name><name xml:lang="ru"><surname>Румянцева</surname><given-names>Т. А.</given-names></name></name-alternatives><email>bgnikon@gmail.com</email><xref ref-type="aff" rid="aff2"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">Ufa Research Institute of Occupational Medicine and Human Ecology</institution></aff><aff><institution xml:lang="ru">Санкт-Петербургский национальный исследовательский университет информационных технологий, механики и оптики</institution></aff></aff-alternatives><aff-alternatives id="aff2"><aff><institution xml:lang="en">Bashkir State Medical University</institution></aff><aff><institution xml:lang="ru">Ярославский государственный медицинский университет</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2021-10-02" publication-format="electronic"><day>02</day><month>10</month><year>2021</year></pub-date><volume>25</volume><issue>3</issue><issue-title xml:lang="en">PULMONOLOGY</issue-title><issue-title xml:lang="ru">ПУЛЬМОНОЛОГИЯ</issue-title><fpage>235</fpage><lpage>242</lpage><history><date date-type="received" iso-8601-date="2021-10-02"><day>02</day><month>10</month><year>2021</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2021, Nikonorova V.G., Chrishtop V.V., Rumyantseva T.A.</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2021, Никонорова В.Г., Криштоп В.В., Румянцева Т.А.</copyright-statement><copyright-year>2021</copyright-year><copyright-holder xml:lang="en">Nikonorova V.G., Chrishtop V.V., Rumyantseva T.A.</copyright-holder><copyright-holder xml:lang="ru">Никонорова В.Г., Криштоп В.В., Румянцева Т.А.</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/><license><ali:license_ref xmlns:ali="http://www.niso.org/schemas/ali/1.0/">http://creativecommons.org/licenses/by/4.0</ali:license_ref></license></permissions><self-uri xlink:href="https://journals.rudn.ru/medicine/article/view/27540">https://journals.rudn.ru/medicine/article/view/27540</self-uri><abstract xml:lang="en"><p style="text-align: justify;">Relevance. Scars are multi-tissue structures that significantly reduce the quality of life of the young, able-bodied population. The most socially significant variants are represented by hypertrophic and keloid postoperative scars and scars after burns, atrophic scars after acne vulgaris and striae. Growth factors, which are also used for their treatment, play a significant role in their formation and progression. The aim of this work is to summarize data on the participation of growth factors (transforming growth factor beta-1 and vascular endothelial growth factor) in the formation of a hypertrophic or atrophic scar. Materials and Methods. The study of literary sources of scientometric scientific bases was carried out. Results and Discussion . The study showed that the duration of the scarring phases preceding it is of great importance in scar formation, their prolongation leads to chronic inflammation and the attachment of an autoimmune component, an increase in the number of myofibroblasts due to inhibition of apoptosis and an increase in the synthesis of intercellular substance and immature forms of collagen, as well as thinning of the epidermis over scar. Growth factors such as growth factor beta-1 and vascular endothelial growth factor are capable of shifting the balance of these two main pathways or towards proliferative processes, contributing to an increase in the number of blood vessels in the hemomicrocirculatory bed, the number of mast cells and total cellularity, as well as, in some cases, the synthesis of keloid - that is, the formation of a hypertrophic or keloid scar. On the contrary, the prevalence of inflammatory processes leads to a decrease in cellularity, a decrease in blood vessels and intercellular substance, as well as damage to elastin and collagen fibers, forming the phenotype of an atrophic scar or striae. Conclusion. Growth factors play a key role in scar formation, contributing to an increase in the number of blood vessels in the hemomicrocirculatory bed, the number of mast cells and total cellularity, as well as, in some cases, the synthesis of keloid - that is, the formation of a hypertrophic or keloid scar.</p></abstract><trans-abstract xml:lang="ru"><p style="text-align: justify;">Актуальность. Рубцы представляют собой мультитканевые структуры, значительно снижающие качество жизни молодого, работоспособного населения. Наиболее социально значимые их варианты представлены гипертрофическими и келлоидными послеоперационными рубцами и рубцами после ожогов, атрофическими рубцами после вульгарных угрей и стриями. Значительную роль в их формировании и прогрессировании играют ростовые факторы, которые так же используются для их лечения. Цель работы: обобщить данные об участии ростовых факторов (трансформирующий фактор роста бета-1 и фактор роста эндотелия сосудов) в формировании рубца по гипертрофическому или атрофическому типу. Материалы и методы . Произведено исследование литературных источников наукометрических научных баз. Результаты и обсуждение . В исследовании показано, что большое значение при формировании рубца имеет длительность предшествующих ему фаз рубцевания, их пролонгация приводит к хронизации воспаления и присоединению аутоимунного компонента, росту количества миофибробластов за счет торможения апоптоза и увеличению синтеза межклеточного вещества и незрелых форм коллагена, а также истончению эпидермиса над рубцом. Ростовые факторы, такие как фактор роста бета-1 и фактора роста эндотелия сосудов способны сдвигать баланс этих двух основных путей или в сторону пролиферативных процессов, способствуя увеличению числа сосудов гемомикроциркуляторного русла, количества тучных клеток и общей клеточности, а также в ряде случаев синтезу келлоида - то есть формированию гипертрофического или келлоидного рубца. Наоборот, превалирование воспалительных процессов приводит к снижению клеточности, уменьшении сосудов и межклеточного вещества, а также повреждению эластиновых и коллагеновых волокон, формируя фенотип атрофического рубца или стрии. Выводы. Ключевую роль в формировании рубца играют факторы роста, способствуя увеличению числа сосудов гемомикроциркуляторного русла, количества тучных клеток и общей клеточности, а также в ряде случаев синтезу келлоида - то есть формированию гипертрофического или келлоидного рубца.</p></trans-abstract><kwd-group xml:lang="en"><kwd>skin</kwd><kwd>scars</kwd><kwd>growth factor beta-1</kwd><kwd>vascular endothelial growth factor</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>кожа</kwd><kwd>рубцы</kwd><kwd>фактор роста бета-1</kwd><kwd>фактора роста эндотелия сосудов</kwd></kwd-group><funding-group/></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Fabbrocini G, Annunziata MC, D’Arco V, De Vita V, Lodi G, Mauriello MC et al. Acne scars: pathogenesis, classification and treatment. Dermatol Res Pract. 2010:893080. doi: 10.1155/2010/893080</mixed-citation></ref><ref id="B2"><label>2.</label><mixed-citation>Kwon HH, Yoon JY, Park SY, Min S, Kim YI, Park JY et al. Activity-guided purification identifies lupeol, a pentacyclic triterpene, as a therapeutic agent multiple pathogenic factors of acne. J Invest Dermatol. 2015;135:1491-500. doi: 10.1038/jid.2015.29</mixed-citation></ref><ref id="B3"><label>3.</label><mixed-citation>Hayashi N, Miyachi Y, Kawashima M. Prevalence of scars and ‘mini-scars’, and their impact on quality of life in Japanese patients with acne. J Dermatol. 2015;42:690-6. doi: 10.1111/1346-8138.12885</mixed-citation></ref><ref id="B4"><label>4.</label><mixed-citation>Disphanurat W, Kaewkes A, Suthiwartnarueput W. Comparison between topical recombinant human epidermal growth factor and Aloe vera gel in combination with ablative fractional carbon dioxide laser as treatment for striae alba: A randomized double-blind trial. Lasers Surg Med. 2020;52(2):166-175. doi: 10.1002/lsm.23052</mixed-citation></ref><ref id="B5"><label>5.</label><mixed-citation>Wolfram D, Tzankov A, Pülzl P, Piza-Katzer H. Hypertrophic scars and keloids - a review of their pathophysiology, risk factors, and therapeutic management. Dermatol Surg. 2009;35(2):171-81. doi: 10.1111/j.1524-4725.2008.34406.x</mixed-citation></ref><ref id="B6"><label>6.</label><mixed-citation>Chun Q, ZhiYong W, Fei S, XiQiao W. Dynamic biological changes in fibroblasts during hypertrophic scar formation and regression. International Wound Journal. 2016;2(13):257-262. doi: 10.1111/iwj.12283</mixed-citation></ref><ref id="B7"><label>7.</label><mixed-citation>Sarrazy V, Billet F, Micallef L, Coulomb B, Desmoulière A. Mechanisms of pathological scarring: Role of myofibroblasts and current developments. Wound Repair and Regeneration. 2011;1(19):10-15. doi: 10.1111/j.1524-475X.2011.00708.x</mixed-citation></ref><ref id="B8"><label>8.</label><mixed-citation>Gökçinar-Yagci B, Uçkan-Çetinkaya D, Çelebi-Saltik B. Pericytes: Properties, functions and applications in tissue engineering. Stem Cell Reviews and Reports. 2015;4(11):549-559. doi: 10.1007/s12015-015-9590-z</mixed-citation></ref><ref id="B9"><label>9.</label><mixed-citation>Ding J, Ma Z, Shankowsky HA, Medina A, Tredget EE. Deep dermal fibroblast profibrotic characteristics are enhanced by bone marrow-derived mesenchymal stem cells. Wound Repair and Regeneration. 2013;3(21):448-455. doi: 10.1111/wrr.12046</mixed-citation></ref><ref id="B10"><label>10.</label><mixed-citation>Kirfel G, Rigort A, Borm B, Schulte C, Herzog V. Structural and compositional analysis of the keratinocyte migration track. Cell Motility and the Cytoskeleton. 2003;1(55):1-13. doi: 10.1002/ cm.10106</mixed-citation></ref><ref id="B11"><label>11.</label><mixed-citation>Oliveira GV, Hawkins HK, Chinkes D, Burke A, Tavares AL et al. Hypertrophic versus non hypertrophic scars compared by immunohistochemistry and laser confocal microscopy: type I and III collagens. Int Wound J. 2009;6(6):445-52. doi: 10.1111/j.1742-481X.2009.00638.x</mixed-citation></ref><ref id="B12"><label>12.</label><mixed-citation>Ulrich D, Ulrich F, Unglaub F, Piatkowski A, Pallua N. Matrix metalloproteinases and tissue inhibitors of metalloproteinases in patients with different types of scars and keloids. J Plast Reconstr Aesthet Surg. 2010;63(6): 1015-1021. doi: 10.1016/j.bjps.2009.04.021</mixed-citation></ref><ref id="B13"><label>13.</label><mixed-citation>Tanzi EL, Alster TS. Laser treatment of scars. Skin Therapy Lett. 2004;9(1):4-7.</mixed-citation></ref><ref id="B14"><label>14.</label><mixed-citation>Xiao A, Ettefagh L. Laser Revision of Scars. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. 2021.</mixed-citation></ref><ref id="B15"><label>15.</label><mixed-citation>Gonzalo-Gil E, Galindo-Izquierdo M. Role of transforming growth factor-beta (TGF-b) in the physiopathology of rheumatoid arthritis. Reumatol Clin. 2014;10(3):174-9. doi: 10.1016/j.reuma.2014.01.009</mixed-citation></ref><ref id="B16"><label>16.</label><mixed-citation>Okamura T, Morita K, Iwasaki Y, Inoue M, Komai T et al. Role of TGF-b3 in the regulation of immune responses. Clin Exp Rheumatol. 2015;33(92):63-9.</mixed-citation></ref><ref id="B17"><label>17.</label><mixed-citation>Lian N, Li T. Growth factor pathways in hypertrophic scars: Molecular pathogenesis and therapeutic implications. Biomedicine and Pharmacotherapy. 2016;(84):42-50. doi: 10.1016/j.biopha.2016.09.010</mixed-citation></ref><ref id="B18"><label>18.</label><mixed-citation>Moon J, Yoo JY, Yan JH, Kwon HH, Min S, Suh DH. Atrophic acne scar: A process from altered metabolism of elastic fibers and collagen fibers based on TGF-β1 signaling. British Journal of Dermatology. 2019;181(6):1226-1237. doi: 10.1111/bjd.17851</mixed-citation></ref><ref id="B19"><label>19.</label><mixed-citation>Filippi CM, Juedes AE, Oldham JE, Ling E, Togher L, Peng Y et al. Transforming growth factor-b suppresses the activation of CD8+ T-cells when naive but promotes their survival and function once antigen experienced: a two-faced impact on autoimmunity. Diabetes. 2008;57(10):2684-92. doi: 10.2337/db08-0609</mixed-citation></ref><ref id="B20"><label>20.</label><mixed-citation>Korn T, Bettelli E, Oukka M, Kuchroo VK. IL-17 and Th17 cells. Annu Rev Immunol. 2009;27:485-517. doi: 10.1146/annurev.immunol.021908.132710</mixed-citation></ref><ref id="B21"><label>21.</label><mixed-citation>Freudlsperger C, Bian Y, Contag Wise S, Burnett J, Coupar J, Yang X et al. TGF-b and NF-jB signal pathway cross-talk is mediated through TAK1 and SMAD7 in a subset of head and neck cancers. Oncogene. 2013;32(12):1549-59. doi: 10.1038/onc.2012.17122. Choi KC, Lee YS, Lim S, Choi HK, Lee CH, Lee EK et al. Smad6 negatively regulates interleukin 1-receptor-Toll-like receptor signalling through direct interaction with the adaptor Pellino-1. Nat Immunol. 2006;7(10):1057-65. doi: 10.1038/ni1383</mixed-citation></ref><ref id="B22"><label>22.</label><mixed-citation>Hong S, Lim S, Li AG, Lee C, Lee YS, Lee EK et al. Smad7 binds to the adaptors TAB2 and TAB3 to block recruitment of the kinase TAK1 to the adaptor TRAF2. Nat Immunol. 2007;8(5);504-13. doi: 10.1038/ni1451</mixed-citation></ref><ref id="B23"><label>23.</label><mixed-citation>Sanjabi S, Zenewicz LA, Kamanaka M, Flavell RA. Anti-inflammatory and pro-inflammatory roles of TGF-b, IL-10, and IL-22 in immunity and autoimmunity. Curr Opin Pharmacol. 2009;9(4):447-53. doi: 10.1016/j.coph.2009.04.008</mixed-citation></ref><ref id="B24"><label>24.</label><mixed-citation>Sato M. Upregulation of the Wnt/β-catenin pathway induced by transforming growth factor-β in hypertrophic scars and keloids. Acta Dermato-Venereologica. 2006;86(4):300-307. doi: 10.2340/000155550101</mixed-citation></ref><ref id="B25"><label>25.</label><mixed-citation>Shah M, Foreman DM, Ferguson MW. Neutralising antibody to TGF-beta 1,2 reduces cutaneous scarring in adult rodents. J Cell Sci. 1994;107(5):1137-57.</mixed-citation></ref><ref id="B26"><label>26.</label><mixed-citation>Xiao Z, Zhang F, Lin W, Zhang M, Liu Y. Effect of Botulinum Toxin Type A on Transforming Growth Factor b1 in Fibroblasts Derived from Hypertrophic Scar: A Preliminary Report. Aesthetic Plast Surg. 2010;34(4):424-427. doi: 10.1007/s00266-009-9423-z</mixed-citation></ref><ref id="B27"><label>27.</label><mixed-citation>Zunwen L, Shizhen Z, Dewu L, Yungui M, Pu N. Effect of tetrandrine on the TGF-β-induced smad signal transduction pathway in human hypertrophic scar fibroblasts in vitro. Burns. 38(3):404-13. doi: 10.1016/j.burns.2011.08.013</mixed-citation></ref><ref id="B28"><label>28.</label><mixed-citation>Zhang YF, Zhou SZ, Cheng XY, Yi B, Shan SZ, Wang J et al. Baicalein attenuates hypertrophic scar formation via inhibition of the transforming growth factor-β/Smad2/3 signalling pathway. British Journal of Dermatology. 2016;1(174):120-130. doi: 10.1111/bjd.14108</mixed-citation></ref><ref id="B29"><label>29.</label><mixed-citation>Bai X, He T, Liu J, Wang Y, Fan L, Tao K et al. Loureirin B inhibits fibroblast proliferation and extracellular matrix deposition in hypertrophic scar via TGF-β/Smad pathway. Experimental Dermatology. 2015;24(5):355-360. doi: 10.1111/exd.12665</mixed-citation></ref><ref id="B30"><label>30.</label><mixed-citation>He T, Bai X, Yang L, Fan L, Li Y, Su L, et al. Loureirin B inhibits hypertrophic scar formation via inhibition of the TGF-beta1ERK/JNK pathway. Cell Physiol. Biochem. 2015;37(2):666-76. doi: 10.1159/000430385</mixed-citation></ref><ref id="B31"><label>31.</label><mixed-citation>Li N, Kong M, Ma T, Gao W, Ma S. Uighur medicine abnormal savda munzip (ASMq) suppresses expression of collagen and TGF-β 1 with concomitant induce Smad7 in human hypertrophic scar fibroblasts. Int J Clin Exp Med. 2015;8(6):8551-60.</mixed-citation></ref><ref id="B32"><label>32.</label><mixed-citation>Qiu SS, Dotor J, Hontanilla B. Effect of P144®(Anti-TGF-β) in an «in Vivo» Human Hypertrophic Scar Model in Nude Mice. PLoS ONE. 2015;10(12): e0144489. doi: 10.1371/journal.pone.0144489</mixed-citation></ref><ref id="B33"><label>33.</label><mixed-citation>Creely JJ, DiMari SJ, Howe AM, Haralson MA. Effects of transforming growth factor-b on collagen synthesis by normal rat kidney epithelial cells. Am J Pathol. 1992;140(1):45-55.</mixed-citation></ref><ref id="B34"><label>34.</label><mixed-citation>La Padula S, Hersant B, Pizza C, Chesné C, Jamin A, Ben Mosbah I et al. Striae Distensae: In Vitro Study and Assessment of Combined Treatment With Sodium Ascorbate and Platelet-Rich Plasma on Fibroblasts. Aesthetic Plast Surg. 2021. doi: 10.1007/s00266-020-02100-7</mixed-citation></ref><ref id="B35"><label>35.</label><mixed-citation>Podobed OV, Prozorovskiĭ NN, Kozlov EA, Tsvetkova TA, Vozdvizhenskiĭ SI, Del’vig AA. Comparative study of collagen in hypertrophic and keloid cicatrix. Vopr Med Khim. 1996;42(3):240-5. (in Russ.)</mixed-citation></ref><ref id="B36"><label>36.</label><mixed-citation>Wollina U, Goldman A. Management of stretch marks (with a focus on striae rubrae). J Cutan Aesthet Surg. 2017;10(3):124-129. doi: 10.4103/JCAS.JCAS_118_17</mixed-citation></ref><ref id="B37"><label>37.</label><mixed-citation>Dreno B, Gollnick HP, Kang S, Thiboutot D, Bettoli V, Torres V et al. Understanding innate immunity and inflammation in acne: implications for management. J Eur Acad Dermatol Venereol. 2015;29(4):3-11. doi: 10.1111/jdv.13190</mixed-citation></ref><ref id="B38"><label>38.</label><mixed-citation>Pardali K, Kowanetz M, Heldin CH, Moustakas A. Smad pathway-specific transcriptional regulation of the cell cycle inhibitor p21(WAF1/Cip1). J Cell Physiol. 2005;204(1):260-72. doi: 10.1002/jcp.20304</mixed-citation></ref><ref id="B39"><label>39.</label><mixed-citation>Albanesi C, Scarponi C, Giustizieri ML, Girolomoni G. Keratinocytes in inflammatory skin diseases. Curr Drug Targets Inflamm Allergy. 2005;4(3):329-34. doi: 10.2174/1568010054022033</mixed-citation></ref><ref id="B40"><label>40.</label><mixed-citation>Werner S, Krieg T, Smola H. Keratinocyte-fibroblast interactions in wound healing. J Invest Dermatol. 2007;127(5):998</mixed-citation></ref><ref id="B41"><label>41.</label><mixed-citation>doi: 10.1038/sj.jid.5700786</mixed-citation></ref><ref id="B42"><label>42.</label><mixed-citation>Johnson KE, Wilgus TA. Vascular Endothelial Growth Factor and Angiogenesis in the Regulation of Cutaneous Wound Repair. Advances in Wound Care. 2014;3(10):647-661. doi: 10.1089/wound.2013.0517</mixed-citation></ref><ref id="B43"><label>43.</label><mixed-citation>Hakvoort T, Altun V, van Zuijlen PP, de Boer WI, van Schadewij WA, van der Kwast TH. Transforming growth factor-beta(1), -beta(2), -beta(3), basic fibroblast growth factor and vascular endothelial growth factor expression in keratinocytes of burn scars. Eur. Cytokine Netw. 2000;11(2):233-239.</mixed-citation></ref><ref id="B44"><label>44.</label><mixed-citation>Zhu KQ, Engrav LH, Armendariz R, Muangman P, Klein MB, Carrougher GJ et al. Changes in VEGF and nitric oxide after deep dermal injury in the female, red Duroc pig - Further similarities between female, Duroc scar and human hypertrophic scar. Burns. 2005;31(1):5-10. doi: 10.1016/j.burns.2004.08.010</mixed-citation></ref><ref id="B45"><label>45.</label><mixed-citation>Chun Q, ZhiYong W, Fei S, XiQiao W. Dynamic biological changes in fibroblasts during hypertrophic scar formation and regression. International Wound Journal. 2016;13(2):257-62. doi: 10.1111/iwj.12283</mixed-citation></ref><ref id="B46"><label>46.</label><mixed-citation>Gaber MA, Seliet IA, Ehsan NA, Megahed MA. Mast cells and angiogenesis in wound healing. Anal Quant Cytopathol Histpathol. 2014;36(1):32-40.</mixed-citation></ref><ref id="B47"><label>47.</label><mixed-citation>Hong YK, Lange-Asschenfeldt B, Velasco P, Hirakawa S, Kunstfeld R, Brown LF et al. VEGF-A promotes tissue repair-associated lymphatic vessel formation via VEGFR-2 and the alpha1beta1 and alpha2beta1 integrins. FASEB Journal. 2004;18(10):1111-3. doi: 10.1096/fj.03-1179fje</mixed-citation></ref><ref id="B48"><label>48.</label><mixed-citation>Brem H, Kodra A, Golinko MS, Entero H, Stojadinovic O, Wang VM et al. Mechanism of sustained release of vascular endothelial growth factor in accelerating experimental diabetic healing. Journal of Investigative Dermatology. 2009;129(9):2275-87. doi: 10.1038/jid.2009.26.</mixed-citation></ref><ref id="B49"><label>49.</label><mixed-citation>Man XY, Yang XH, Cai SQ, Yao YG, Zheng M. Immunolocalization and expression of vascular endothelial growth factor receptors (VEGFRs) and neuropilins (NRPs) on keratinocytes in human epidermis. Mol. Med. 2006;12(7-8):127-36. doi: 10.2119/2006-00024.Man</mixed-citation></ref><ref id="B50"><label>50.</label><mixed-citation>Zhu JW, Wu XJ, Luo D, Lu ZF, Cai SQ, Zheng M. Activation of VEGFR-2 signaling in response to moderate dose of ultraviolet B promotes survival of normal human keratinocytes. International Journal of Biochemistry and Cell Biology. 2012;44(1):246-56. doi: 10.1016/j.biocel.2011.10.022</mixed-citation></ref><ref id="B51"><label>51.</label><mixed-citation>Khanna S, Biswas S, Shang Y, Collard E, Azad A, Kauh C et al. Macrophage dysfunction impairs resolution of inflammation in the wounds of diabetic mice. PLoS One. 2010;5(3): e9539. doi: 10.1371/journal.pone.0009539</mixed-citation></ref><ref id="B52"><label>52.</label><mixed-citation>Mirza R, Koh TJ. Dysregulation of monocyte/macrophage phenotype in wounds of diabetic mice. Cytokine. 2011;56(2):256-64. doi: 10.1016/j.cyto.2011.06.016</mixed-citation></ref><ref id="B53"><label>53.</label><mixed-citation>Wilgus TA, Ferreira AM, Oberyszyn TM, Bergdall VK, Dipietro LA. Regulation of scar formation by vascular endothelial growth factor. Lab Invest. 2008;88(6):579-90. doi: 10.1038/labinvest.2008.36</mixed-citation></ref><ref id="B54"><label>54.</label><mixed-citation>Wang Z, Shi C. Cellular senescence is a promising target for chronic wounds: a comprehensive review. Burns &amp; Trauma. 2020;(8):8: tkaa021. doi: 10.1093/burnst/tkaa021</mixed-citation></ref><ref id="B55"><label>55.</label><mixed-citation>Konstantinova MV, Vasiliev AG, Verlov NA, Artyomenko MR. Boosting Angiogenesis in Skin Mechanical Trauma Area by means of Neoskin Skin-Substitute Preparation. Pediatrician (St. Petersburg). 2016;7(2):85-91. doi: 10.17816/PED7285-91. (in Russ.)</mixed-citation></ref><ref id="B56"><label>56.</label><mixed-citation>Zacchigna S, Tasciotti E, Kusmic C, Arsic N, Sorace O, Marini C et al. In vivo imaging shows abnormal function of vascular endothelial growth factorinduced vasculature. Hum. Gene Ther. 2007;18(6):515-24. doi: 10.1089/hum.2006.162</mixed-citation></ref><ref id="B57"><label>57.</label><mixed-citation>Bluff JE, O’Ceallaigh S, O’Kane S, Ferguson MW, Ireland G. The microcirculation in acute murine cutaneous incisional wounds shows a spatial and temporal variation in the functionality of vessels. Wound Repair and Regeneration. 2006;14(4):434-42. doi: 10.1111/j.1743-6109.2006.00142.x</mixed-citation></ref><ref id="B58"><label>58.</label><mixed-citation>Benjamin LE, Golijanin D, Itin A, Pode D, Keshet E. Selective ablation of immature blood vessels in established human tumors follows vascular endothelial growth factor withdrawal. Journal of Clinical Investigation. 1999;103(2):159-65. doi: 10.1172/JCI5028</mixed-citation></ref><ref id="B59"><label>59.</label><mixed-citation>Iglin VA, Sokolovskaya OA, Morozova SM, Kuchur OA, Nikonorova VG, Sharsheeva A et al. Effect of Sol-Gel Alumina Biocomposite on the Viability and Morphology of Dermal Human Fibroblast Cells. ACS Biomaterials Science and Engineering. 2020;6(8):4397-4400. doi: 10.1021/acsbiomaterials.0c00721</mixed-citation></ref></ref-list></back></article>
