jsmsJournal of Siberian Medical SciencesJournal of Siberian Medical Sciences2542-1174Federal state budgetary educational institution of higher education "Novosibirsk state medical university" of Ministry of Health of the Russian Federation (FSBEI HE NSMU MOH Russia)10.31549/2542-1174-2020-2-98-110jsms-632Research ArticleОБЗОРЫREVIEWГенетическая предрасположенность к формированию рубцов при акнеGenetic predisposition to the formation of acne scarsНемчаниноваО. Б.NemchaninovaO. B.

д-р мед. наук, профессор, заведующий кафедрой дерматовенерологии и косметологии,

Новосибирск

Dr. Sci. (Med.), Professor, Head, Department of Dermatovenereology and Cosmetology, 

Novosibirsk 

ЧерниковаЕ. В.ChernikovaE. V.

канд. мед. наук, ассистент кафедры дерматовенерологии и косметологии,

630091, г. Новосибирск, Красный просп., 52

Cand. Sci. (Med.), Assistant, Department of Dermatovenereology and Cosmetology, 

52, Krasny Prospect, Novosibirsk, 630091

evchernikova@mail.ruМаксимоваЮ. В.MaksimovaYu. V.

д-р мед. наук, профессор, заведующий кафедрой медицинской генетики и биологии,

Новосибирск

Dr. Sci. (Med.), Professor, Head, Department of Medical Genetics and Biology,

Novosibirsk

РешетниковаТ. Б.ReshetnikovaT. B.

д-р мед. наук, профессор кафедры дерматовенерологии и косметологии,

Новосибирск

Dr. Sci. (Med.), Professor, Department of Dermatovenereology and Cosmetology,

Novosibirsk

СпицынаА. В.SpitsynaA. V.

канд. мед. наук, доцент кафедры дерматовенерологии и косметологии,

Новосибирск

Cand. Sci. (Med.), Associate Professor, Department of Dermatovenereology and Cosmetology,

Novosibirsk

МаксимовВ. Н.MaksimovV. N.

д-р мед. наук, профессор, заведующий лабораторией молекулярно-генетических исследований терапевтических заболеваний,

Новосибирск

Dr. Sci. (Med.), Professor, Head, Laboratory of Molecular Genetic Research of Therapeutic Diseases,

Novosibirsk

ФГБОУ ВО «Новосибирский государственный медицинский университет» Минздрава РоссииРоссияNovosibirsk State Medical UniversityRussian FederationФГБОУ ВО «Новосибирский государственный медицинский университет» Минздрава России; НИИ терапии и профилактической медицины — филиал ФГБНУ «Федеральный исследовательский центр Институт цитологии и генетики Сибирского отделения Российской академии наук»Russian FederationNovosibirsk State Medical University; Research Institute of Internal and Preventive Medicine (Novosibirsk)Russian Federation2020300620200298110Copyright © Немчанинова О.Б., Черникова Е.В., Максимова Ю.В., Решетникова Т.Б., Спицына А.В., Максимов В.Н., 20202020Немчанинова О.Б., Черникова Е.В., Максимова Ю.В., Решетникова Т.Б., Спицына А.В., Максимов В.Н.Nemchaninova O.B., Chernikova E.V., Maksimova Y.V., Reshetnikova T.B., Spitsyna A.V., Maksimov V.N.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://jsms.elpub.ru/jour/article/view/632

Обзор литературы посвящен ассоциациям молекулярно-генетических маркеров с процессом образования рубцов у пациентов с акне. С учетом высокой распространенности заболевания и долгосрочных негативных эстетических последствий проблема постакне представляется очень актуальной. Однако обнаружение надежных прогностических маркеров повышенного риска формирования рубцов на фоне акне остается на сегодняшний день нерешенной задачей. В обзоре рассмотрено большинство современных публикаций с результатами анализа ассоциации молекулярно-генетических маркеров с рубцами постакне, из которых следует, что изучение генетических аспектов формирования рубцов у пациентов с акне находится практически на самом начальном этапе. Отсутствие эффективных средств профилактики и лечения рубцов постакне обусловливает необходимость дальнейшего поиска.

The paper presents a literature review on the associations of molecular genetic markers with scar formation in patients with acne. Given the high prevalence of the disease and long-term negative aesthetic consequences, the problem of post-acne is very relevant. However, the detection of reliable prognostic markers of an increased risk of scar formation due to acne is remaining an unsolved problem. The paper reviews most recent publications devoted to the analysis of molecular genetic markers with post-acne scars and concluded that the study of the genetic aspects of scar formation in patients with acne is almost at the initial stage. The lack of effective means for the prevention and treatment of acne scars necessitates a further search.

рубецкелоидакнегенполиморфизмоднонуклеотидный полиморфизмscarkeloidacnegenepolymorphismsingle nucleotide polymorphismReferencesХёгер П.Г. Детская дерматология: пер. с нем. / под ред. А.А. Кубановой, А.Н. Львова. М.: Изд-во Панфилова; БИНОМ, 2013. 648 с.Höger P.G. (2013). Pediatric Dermatology. (A.A. Kubanova, A.N. Lvova, Trans.). Moscow: Publishing House of Panfilov; BINOM, 648 p. In Russ.Thiboutot D.M., Dréno B., Abanmi A. et al. Practical management of acne for clinicians: An international consensus from the Global Alliance to Improve Outcomes in Acne // J. Am. Acad. Dermatol. 2018. Vol. 78 (2, 1). P. S1–S23.e1. doi: 10.1016/j.jaad.2017.09.078.Thiboutot D.M., Dréno B., Abanmi A. (2018). Practical management of acne for clinicians: An international consensus from the Global Alliance to Improve Outcomes in Acne. J. Am. Acad. Dermatol., 78 (2, 1), S1–S23.e1. doi: 10.1016/j.jaad.2017.09.078.Dréno B., Bagatin E., Blume-Peytavi U. et al. Female type of adult acne: Physiological and psychological considerations and management // J. Dtsch. Dermatol. Ges. 2018 Oct. Vol. 16 (10). P. 1185–1194.Dréno B., Bagatin E., Blume-Peytavi U. et al. (2018, Oct). Female type of adult acne: Physiological and psychological considerations and management. J. Dtsch. Dermatol. Ges., 16 (10), 1185–1194. In Germ.Harper J.C., Stein Gold L.F., Alexis A.F., Tan J.K.L. Treating acne in adult women // Semin. Cutan. Med. Surg. 2018 Jun. Vol. 37 (3S). P. S67–S70.Harper J.C., Stein Gold L.F., Alexis A.F., Tan J.K.L. (2018, Jun). Treating acne in adult women. Semin. Cutan. Med. Surg., 37 (3S), S67–70.Connolly D., Vu H.L., Mariwalla K., Saedi N. Acne scarring — pathogenesis, evaluation, and treatment options // J. Clin. Aesthet. Dermatol. 2017. Vol. 10 (9). P. 12–23.Connolly D., Vu H.L., Mariwalla K., Saedi N. (2017). Acne scarring — pathogenesis, evaluation, and treatment options. J. Clin. Aesthet. Dermatol., 10 (9), 12–23.Carlavan I., Bertino B., Rivier M. et al. Atrophic scar formation in patients with acne involves long-acting immune responses with plasma cells and alteration of sebaceous glands // Br. J. Dermatol. 2018 Oct. Vol. 179 (4). P. 906–917. doi: 10.1111/bjd.16680.Carlavan I., Bertino B., Rivier M. et al. (2018, Oct). Atrophic scar formation in patients with acne involves long-acting immune responses with plasma cells and alteration of sebaceous glands. Br. J. Dermatol., 179 (4), 906–917. doi: 10.1111/bjd.16680.Tan J., Thiboutot D., Gollnick H. et al. Development of an atrophic acne scar risk assessment tool // J. Eur. Acad. Dermatol. Venereol. 2017 Sep. Vol. 31 (9). P. 1547– 1554. doi: 10.1111/jdv.14325.Tan J., Thiboutot D., Gollnick H. et al. (2017, Sep). Development of an atrophic acne scar risk assessment tool. J. Eur. Acad. Dermatol. Venereol., 31 (9), 1547– 1554. doi: 10.1111/jdv.14325.Kang S., Lozada V.T., Bettoli V. et al. New atrophic acne scar classifi cation: reliability of assessments based on size, shape, and number // J. Drugs Dermatol. 2016 Jun 1. Vol. 15 (6). P. 693–702.Kang S., Lozada V.T., Bettoli V. et al. (2016, Jun 1). New atrophic acne scar classification: reliability of assessments based on size, shape, and number. J. Drugs Dermatol., 15 (6), 693–702.Tan J., Bourdés V., Bissonnette R. et al. Prospective study of pathogenesis of atrophic acne scars and role of macular erythema // J. Drugs Dermatol. 2017 Jun 1. Vol. 16 (6). P. 566–572.Tan J., Bourdés V., Bissonnette R. et al. (2017, Jun 1). Prospective study of pathogenesis of atrophic acne scars and role of macular erythema. J. Drugs Dermatol., 16 (6), 566–572.Lee H.J., Jang Y.J. Recent understandings of biology, prophylaxis and treatment strategies for hypertrophic scars and keloids // Int. J. Mol. Sci. 2018. Vol. 19 (3). P. 711. doi: 10.3390/ijms19030711.Lee H.J., Jang Y.J. (2018). Recent understandings of biology, prophylaxis and treatment strategies for hypertrophic scars and keloids. Int. J. Mol. Sci., 19 (3), 711. doi: 10.3390/ijms19030711.Tan S., Khumalo N., Bayat A. Understanding keloid pathobiology from a quasi-neoplastic perspective: less of a scar and more of a chronic infl ammatory disease with cancer-like tendencies // Front. Immunol. 2019. Vol. 10. P. 1810. doi: 10.3389/fimmu.2019.01810.Tan S., Khumalo N., Bayat A. (2019). Understanding keloid pathobiology from a quasi-neoplastic perspective: less of a scar and more of a chronic inflammatory disease with cancer-like tendencies. Front. Immunol., 10, 1810. doi: 10.3389/fimmu.2019.01810.Zhu Z., Ding J., Tredget E.E. The molecular basis of hypertrophic scars // Burns & Trauma. 2016. Vol. 4. P. 2. doi: 10.1186/s41038-015-0026-4.Zhu Z., Ding J., Tredget E.E. (2016). The molecular basis of hypertrophic scars. Burns & Trauma, 4, 2. doi: 10.1186/s41038-015-0026-4. 13. Tuan T.L., Nichter L.S. (1998). The molecular basis of keloid and hypertrophic scar formation. Mol. Med. Today, 4, 19–24. doi: 10.1016/S1357-4310(97) 80541-2.Tuan T.L., Nichter L.S. The molecular basis of keloid and hypertrophic scar formation // Mol. Med. Today. 19 98. Vol. 4. P. 19–24. doi: 10.1016/S1357-4310(97)80541-2.Krumdieck R., Hook M., Rosenberg L.C., Volanakis J.E. (1992). The proteoglycan decorin binds C1q and inhibits the activity of the C1 complex. J. Immunol., 149, 3695–3701.Krumdieck R., Hook M., Rosenberg L.C., Volanakis J.E. The proteoglycan decorin binds C1q and inhibits the activity of the C1 complex // J. Immun ol. 1992. Vol. 149. P. 3695–3701.Wang P., Liu X., Xu P. et al. (2016). Decorin reduces hypertrophic scarring through inhibition of the TGF-β1/Smad signalling pathway in a rat osteomyelitis model. Exp. Ther. Med., 12 (4), 2102–2108. doi: 10.3892/etm.2016.3591.Wang P., Liu X., Xu P. et al. Decorin reduces hypertrophic scarring through inhibition of the TGF-β1/Smadsignalin g pathway in a rat osteomyelitis model // Exp. Ther. Med. 2016. Vol. 12 (4). P. 2102–2108. doi: 10.3892/etm.2016.3591.Yokota K., Kobayakawa K., Saito T. et al. (2017, Mar). Periostin promotes scar formation through the interaction between pericytes and infiltrating monocytes/macrophages after spinal cord injury. Am. J. Pathol., 187 (3), 639–653. doi: 10.1016/j.ajpath.2016.11.010.Yokota K., Kobayakawa K., Saito T. et al. Periostin pro motes scar formation through the interaction between pericytes and infiltrating monocytes / macrophages after spinal cord injury // Am. J. Pathol. 2017 Mar. Vol. 187 (3). P. 639–653. doi: 10.1016/j.ajpath.2016.11.010.Crawford J., Nygard K., Gan B.S., O’Gorman D.B. (2015, Feb). Periostin induces fibroblast proliferation and myofibroblast persistence in hypertrophic scarring. Exp. Dermatol., 24 (2), 120–126. doi: 10.1111/ exd.12601.Crawford J., Nygard K., Gan B.S., O’Gorman D.B. Periostin induces fibroblast proliferation and myofi broblast persistence in hypertrophic scarring // Exp. Dermatol. 2015 Feb. Vol. 24 (2). P. 120–126. doi: 10.1111/exd.12601.Akoglu G., Tan C., Ayvaz D.C., Tezcan I. (2019, Feb). Tumour necrosis factor α-308 G/A and interleukin 1 β-511 C/T gene polymorphisms in patients with scarring acne. J. Cosmet. Dermatol., 18 (1), 395–400. doi: 10.1111/jocd.12558.Akoglu G., Tan C. , Ayvaz D.C., Tezcan I. Tumor necrosis factor α-308 G/A and interleukin 1 β-511 C/T gene polymorphisms in patients with scarring acne // J. Cosmet. Dermatol. 2019 Feb. Vol. 18 (1). P. 395– 400. doi: 10.1111/jocd.12558.Ogawa R. (2017, Mar). Keloid and hypertrophic scars are the result of chronic inflammation in the reticular dermis. Int. J. Mol. Sci., 18 (3), pii: E606. doi: 10.3390/ijms18030606.Ogawa R. Keloid and hypertrophic scars are the result of chronic inflammation in the reticular dermis // Int. J. Mol. Sci. 2017 Mar 10. Vol. 18 (3). pii: E606. doi: 10.33 90/ijms18030606.Velez Edwards D.R., Tsosie K.S., Williams S.M. et al. (2014, Dec). Admixture mapping identifies a locus at 15q21.2-22.3 associated with keloid formation in African Americans. Hum. Genet., 133 (12), 1513–1523. doi: 10.1007/s00439-014-1490-9.Velez Edwards D.R., Tsosie K.S., Williams S.M. et al. Admixture mapping identifi es a locus at 15q21.2-22.3 associated with keloid formation in African Americans // Hum. Genet. 2014 Dec . Vol. 133 (12). P. 1513– 1523. doi: 10.1007/s00439-014-1490-9.HuGE Navigator. URL: https://phgkb.cdc.gov/PHGKB/startPagePhenoPedia.action.HuGE Navigator. URL: https://phgkb.cdc.gov/PHGKB/startPagePhenoPedia.action.Wang R., Ghahary A., Shen Q. et al. (2000, Mar-Apr). Hypertrophic scar tissues and fibroblasts produce more transforming growth factor-beta1 mRNA and protein than normal skin and cells. Wound Repair Regen., 8 (2), 128–137.Wang R., Ghahary A., Shen Q. et al. Hypertrophic scar tissues and fibroblasts produce more transforming growth factor-be ta1 mRNA and protein than normal skin and cells // Wound Repair Regen. 2000 Mar-Apr. Vol. 8 (2). P. 128–137.Song M., Liu Y. (2014, Dec). Analysis on polymorphism at -509 C/T site of TGF-β1 gene in patients with keloids. Zhonghua Shao Shang Za Zhi, 30 (6), 482–486.Song M., Liu Y. Analysis on polym orphism at -509 C/T site of TGF-β1 gene in patients with keloids // Zhonghua Shao Shang Za Zhi. 2014 Dec. Vol. 30 (6). P. 482–486.Tu Y., Lineaweaver W.C., Zhang F. (2017, May 29). TGF-β1 -509C/T polymorphism and susceptibility to keloid disease: a systematic review and meta-analysis. Scars, Burns & Heal, 3. doi: 10.1177/2059513117709943.Tu Y., Lineaweaver W.C., Zhang F. TGF -β1 -509C/T polymorphism and susceptibility to keloid disease: a systematic review and meta-analysis // Scars, Burns & Heal. 2017 May 29. Vol. 3. doi: 10.1177/2059513117709943.Zhu X.J., Li W.Z., Li H. et al. (2017, Apr 20). Association of interleukin-6 gene polymorphisms and circulating levels with keloid scars in a Chinese Han population. Genet. Mol. Res., 16 (2). doi: 10.4238/gmr16029110.Zhu X.J., Li W.Z., Li H. et al. Association of interleukin-6 gene polymorphisms and circulating levels with keloid scars in a Chinese Han population // Genet. Mol. Res. 2017 Apr 20. Vol. 16 (2). doi: 10.4238/gmr16029110.Shih B., Bayat A. (2012, Apr). Comparative genomic hybridisation analysis of keloid tissue in Caucasians suggests a possible involvement of HLA-DRB5 in disease pathogenesis. Arch. Dermatol. Res., 304 (3), 241–249. doi: 10.1007/s00403-011-1182-4.Shih B., Bayat A. Comparative genomic hybridisation analysis of keloid tissue in Caucasians suggests possible involvement of HLA-DRB5 in disease pathogenesis // Arch. Dermatol. Res. 2012 Apr. Vol. 304 (3). P. 241–249. doi: 10.1007/s00403-011-1182-4.Wu Y., Wang B., Li Y.H. et al. (2012, Jun 29). Meta-analysis demonstrates an association between Arg72Pro polymorphism in the P53 gene and susceptibility to keloids in the Chinese population. Genet. Mol. Res., 11 (2), 1701–1711. doi: 10.4238/2012.Wu Y., Wang B., Li Y.H. et al. Meta-analysis demonstrates association between Arg72Pro polymorphism in the P53 gene and susceptibility to keloids in the Chinese population // Genet. Mol. Res. 2012 Jun 29. Vol. 11 (2). P. 1701–1711. doi: 10.4238/2012.He L., Wu W.J., Yang J.K. et al. (2014). Two new susceptibility loci 1q24.2 and 11p11.2 confer risk to severe acne. Nat. Commun., 5, 2870.He L., Wu W.J., Yang J.K. et al. Two new susceptibility loci 1q24.2 and 11p11.2 confer risk to severe acne // Nat. Commun. 2014. Vol. 5: 2870.Nakashima M., Chung S., Takahashi A. et al. (2010, Sep). A genome-wide association study identifies four susceptibility loci for keloid in the Japanese population. Nat. Genet., 42 (9), 768–771. doi: 10.1038/ng.645.Nakashima M., Chung S., Takahashi A. et al. A genome-wide association study identifi es four susceptibility loc i for keloid in the Japanese population // Nat. Genet. 2010 Sep. Vol. 42 (9). P. 768–771. doi: 10.1038/ng.645.Zhu F., Wu B., Li P. et al. (2013, May 7). Association study confirmed susceptibility loci with keloid in the Chinese Han population. PLoS One, 8 (5): e62377. doi: 10.1371/journal.pone.0062377.Zhu F., Wu B., Li P. et al. Association study confi rmed susceptibility loci with keloid in the Chinese Han population // PLoS One. 2013 May 7. Vol. 8 (5): e62377. doi: 10.1371/journal.pone.0062377.Fujita M., Yamamoto Y., Jiang J.J. et al. (2019, Feb). NEDD4 is involved in inflammation development during keloid formation. J. Invest. Dermatol., 139 (2), 333–341. doi: 10.1016/j.jid.2018.07.044.Fujita M., Yamamoto Y., Jiang J.J. et al. NEDD4 is involved in inflammation development during keloid formation // J. Invest. Dermatol. 2019 Feb. Vol. 139 (2). P. 333–341. doi: 10.1016/j.jid.2018.07.044.Chen L., Li J., Li Q. et al. (2018). Overexpression of LncRNA AC067945.2 down-regulates collagen expression in skin fibroblasts and possibly correlates with the VEGF and Wnt signalling pathways. Cell. Physiol. Biochem., 45 (2), 761–771. doi: 10.1159/000487167.Chen L., Li J., Li Q. et al. Overexpression of LncRNA AC067945.2 down-regulates collagen expression in skin fi broblasts and possibly correlates with the VEGF and Wnt signalling pathways // Cell. Physiol. Biochem. 2018. Vol. 45 (2) . P. 761–771. doi: 10.1159/000487167.Li J., Chen L., Cao C. et al. (2016). The long non-coding RNA LncRNA8975-1 is upregulated in hypertrophic scarfibroblasts and controls collagen expression. Cell. Physiol. Biochem., 40 (1–2), 326–334.Li J., Chen L., Cao C. et al. The long non-coding RNA LncRNA8975-1 is upregulated in hypertrophic scar fi broblasts and controls collagen expression // Cell. Physiol. Biochem. 2016. Vol. 40 (1–2). P. 326–334.Wu X., Li J., Yang X. et al. (2018, Aug). MiR-155 inhibits the formation of hypertrophic scar fi broblasts by targeting HIF-1α via PI3K/AKT pathway. J. Mol. Histol., 49 (4), 377–387. doi: 10.1007/s10735-018-9778-z.Wu X., Li J., Yang X. et al. miR-155 inhibits the formation of hypertrophic scar fi broblasts by targeting HIF-1α via PI3K/AKT pathway / / J. Mol. Histol. 2018 Aug. Vol. 49 (4). P. 377–387. doi: 10.1007/s10735-018-9778-z.Wang X., Zhang Y., Jiang B.H. et al. (2017, Dec 15). Study on the role of Hsa-miR-31-5p in hypertrophic scar formation and the mechanism. Exp. Cell. Res., 361 (2), 201–209. doi: 10.1016/j.yexcr.2017.09.009.Wang X., Zhang Y., Jiang B.H. et al. Study on the role of Hsa-miR-31-5p in hypertrophic scar formation and the mechanism // Exp. Cell. R es. 2017 Dec 15. Vol. 361 (2). P. 201–209. doi: 10.1016/j.yexcr.2017.09.009.Marshall C.D., Hu M.S., Leavitt T. et al. (2018, Feb 1). Cutaneous scarring: basic science, current treatments, and future directions. Adv. Wound Care (New Rochelle), 7 (2), 29–45. doi: 10.1089/wound.2016.0696.Marshall C.D., Hu M.S., Leavitt T. et al. Cutaneous scarring: basic science, current treatments, and future directions // Adv. Wound Care (New Rochelle). 2018 Feb 1. Vol. 7 ( 2). P. 29–45. doi: 10.1089/wound.2016.0696.Chen L., Li J., Li Q. et al. (2017, Aug). Non-coding RNAs: the new insight on hypertrophic scar. J. Cell. Biochem., 118 (8), 1965–1968. doi: 10.1002/jcb.25873.Chen L., Li J., Li Q. et al. Non-coding RNAs: the new insight on hypertrophic scar // J. Cell. Biochem. 2017 Aug. Vol. 118 (8). P. 1965–1968. doi: 10.1002/jcb.25873.Chen L., Li J., Li Q. et al. Non-coding RNAs: the new insight on hypertrophic scar // J. Cell. Biochem. 2017 Aug. Vol. 118 (8). P. 1965–1968. doi: 10.1002/jcb.25873.

The authors declare that there are no conflicts of interest present.