转录因子和受体调控痤疮发病机制的研究进展

doi:10.35541/cjd.20210457

中华皮肤科杂志 ›› 2022, e20210457.doi: 10.35541/cjd.20210457

转录因子和受体调控痤疮发病机制的研究进展

封梦荻王文氢

河北医科大学第四医院皮肤科，石家庄 050000

收稿日期:2021-06-21 修回日期:2021-11-02 发布日期:2022-08-01
通讯作者: 王文氢 E-mail:wwqbio@163.com
作者简介:4月份能否先期发表

Regulatory roles of transcription factors and receptors in the pathogenesis of acne

Feng Mengdi, Wang Wenqing

Department of Dermatology, The Fourth Hospital of Hebei Medical University, Shijiazhuang 050000, China

Received:2021-06-21 Revised:2021-11-02 Published:2022-08-01
Contact: Wang Wenqing E-mail:wwqbio@163.com

摘要/Abstract

摘要： 【摘要】痤疮的发病机制尚不完全明确。目前已肯定了转录因子和受体在痤疮发生发展中的作用，其中Toll样受体、胰岛素样生长因子、雄激素受体是痤疮的危险因素，而维生素D、维A酸受体、表皮生长因子、过氧化物酶体增殖物激活受体是保护因素，这些因子有望成为痤疮预防和治疗的靶点。本文综述近年来痤疮相关的转录因子及其受体的研究进展，为痤疮的靶向治疗提供新方向。

关键词: 寻常痤疮, 转录因子, 转录因子受体, 发病机制, 信号转导通路

Abstract: 【Abstract】 The pathogenesis of acne is still unclear. At present, studies have confirmed roles of transcription factors and receptors in the occurrence and development of acne. Toll-like receptors, insulin-like growth factors, androgen receptors are risk factors for acne, while vitamin D receptors, retinoic acid receptors, epidermal growth factors, peroxisome proliferator-activator receptors are protective factors for acne, all of which are expected to be targets for prevention and treatment of acne. This review focuses on recent research progress in acne-related transcription factors and their receptors, in order to provide new directions for targeted therapy of acne.

Key words: Acne vulgaris, Transcription factors, Receptor of transcription factors, Pathogenesis, Signaling transduction pathway

封梦荻王文氢. 转录因子和受体调控痤疮发病机制的研究进展[J]. 中华皮肤科杂志, 2022,e20210457. doi:10.35541/cjd.20210457

Feng Mengdi, Wang Wenqing. Regulatory roles of transcription factors and receptors in the pathogenesis of acne[J]. Chinese Journal of Dermatology,2022,e20210457. doi:10.35541/cjd.20210457

参考文献 36

［1］	中国痤疮治疗指南专家组. 中国痤疮治疗指南（2019修订版）［J］. 临床皮肤科杂志, 2019,48（9）:583⁃588. doi: 10.16761/j.cnki.1000⁃4963.2019.09.020.
［2］	Yang S, Fang F, Yu X, et al. Knockdown of H19 inhibits the pathogenesis of acne vulgaris by targeting the mir⁃196a/TLR2/NF⁃κB axis［J］. Inflammation, 2020,43（5）:1936⁃1947. doi: 10.1007/s10753⁃020⁃01268⁃z.
［3］	Fernández JR, Webb C, Rouzard K, et al. SIG1459: a novel phytyl⁃cysteine derived TLR2 modulator with in vitro and clinical anti⁃acne activity［J］. Exp Dermatol, 2018,27（9）:993⁃999. doi: 10.1111/exd.13692.
［4］	樊莎莎, 丁杨, 方慧倩, 等. 痤疮患者血清中多态上皮黏液素和TolL样受体信号表达活化与患者病情的关系［J］. 中国卫生检验杂志, 2020,30（12）:1476⁃1478.
［5］	Suvanprakorn P, Tongyen T, Prakhongcheep O, et al. Establishment of an anti⁃acne vulgaris evaluation method based on TLR2 and TLR4⁃mediated interleukin⁃8 production［J］. In Vivo, 2019,33（6）:1929⁃1934. doi: 10.21873/invivo.11687.
［6］	Suvanprakorn P, Tongyen T, Prakhongcheep O, et al. Establishment of an anti⁃acne vulgaris evaluation method based on TLR2 and TLR4⁃mediated interleukin⁃8 production［J］. In Vivo, 2019,33（6）:1929⁃1934. doi: 10.21873/invivo.11687.
［7］	El⁃Tahlawi S, Ezzat Mohammad N, Mohamed El⁃Amir A, et al. Survivin and insulin⁃like growth factor⁃I: potential role in the pathogenesis of acne and post⁃acne scar［J］. Scars Burn Heal, 2019,5:20595131 18818031. doi: 10.1177/2059513118818031.
［8］	Briganti S, Flori E, Mastrofrancesco A, et al. Acne as an altered dermato⁃endocrine response problem ［J］. Exp Dermatol, 2020, 29（9）: 833⁃839, doi:10.1111/exd.14168.
［9］	Behrangi E, Rasi A, Navid P, et al. Serum level of insulin⁃like growth factor 1 in patients with acne vulgaris versus healthy subjects［J］. J Skin Stem Cell, 2018,5（3）:e79784. doi: 10.5812/jssc.79784.
［10］	Rodighiero E, Bertolani M, Saleri R, et al. Do acne treatments affect insulin⁃like growth factor⁃1 serum levels? A clinical and laboratory study on patients with acne vulgaris［J］. Dermatol Ther, 2020,33（3）:e13439. doi: 10.1111/dth.13439.
［11］	Rahaman S, De D, Handa S, et al. Association of insulin⁃like growth factor （IGF）⁃1 gene polymorphisms with plasma levels of IGF⁃1 and acne severity［J］. J Am Acad Dermatol, 2016,75（4）:768⁃773. doi: 10.1016/j.jaad.2016.05.019.
［12］	Zinati⁃Saeed S, Shakiba E, Rahimi Z, et al. The insulin⁃like growth factor⁃1 （G>A） and 5,10⁃methylenetetrahydrofolate reductase （C677T） gene variants and the serum levels of insulin⁃like growth factor⁃1, insulin, and homeostasis model assessment in patients with acne vulgaris［J］. Iran J Pathol, 2020,15（1）:23⁃29. doi: 10.30699/IJP.2019.105695.2098.
［13］	Ceruti JM, Leirós GJ, Balañá ME. Androgens and androgen receptor action in skin and hair follicles［J］. Mol Cell Endocrinol, 2018,465:122⁃133. doi: 10.1016/j.mce.2017.09.009.
［14］	Bansal P, Sardana K, Sharma L, et al. A prospective study examining isolated acne and acne with hyperandrogenic signs in adult females［J］. J Dermatolog Treat, 2021,32（7）:752⁃755. doi: 10.1080/09546634.2019.1708245.
［15］	Demirkan S, Sayın DB, Gündüz Ö. CAG polymorphism in the androgen receptor gene in women may be associated with nodulocystic acne［J］. Postepy Dermatol Alergol, 2019,36（2）:173⁃176. doi: 10.5114/ada.2019.84592.
［16］	Bharti S, Vadlamudi HC. A strategic review on the involvement of receptors, transcription factors and hormones in acne pathogenesis［J］. J Recept Signal Transduct Res, 2021,41（2）:105⁃116. doi: 10.1080/10799893.2020.1805626.
［17］	El⁃Hamd MA, El Taieb MA, Ibrahim HM, et al. Vitamin D levels in acne vulgaris patients treated with oral isotretinoin［J］. J Cosmet Dermatol, 2019,18（1）:16⁃20. doi: 10.1111/jocd.12503.
［18］	Umar M, Sastry KS, Al Ali F, et al. Vitamin D and the pathophysiology of inflammatory skin diseases［J］. Skin Pharmacol Physiol, 2018,31（2）:74⁃86. doi: 10.1159/000485132.
［19］	Swelam MM, El⁃Barbary R, Saudi WM, et al. Associations among two vitamin D receptor （VDR） gene polymorphisms （ApaI and TaqI） in acne vulgaris: a pilot susceptibility study［J］. J Cosmet Dermatol, 2019,18（4）:1113⁃1120. doi: 10.1111/jocd.12781.
［20］	Kemeriz F, Tuncer SÇ, Acar EM, et al. Evaluation of 25⁃hydroxy vitamin D levels and disease severity in patients with acne vulgaris［J］. Dermatol Ther, 2020,33（3）:e13393. doi: 10.1111/dth.13393.
［21］	Ahmed Mohamed A, Salah Ahmed E M, Abdel⁃Aziz R T A, et al. The impact of active vitamin D administration on the clinical outcomes of acne vulgaris ［J］. J Dermatolog Treat, 2020:1⁃6. doi:10.1080/09546634.2019.1708852.
［22］	Al⁃Taiar A, Alkhabbaz M, Rahman A, et al. Plasma 25⁃hydroxy vitamin D is not associated with acne vulgaris［J］. Nutrients, 2018,10（10）:15⁃25, doi:10.3390/nu10101525.
［23］	Kassir M, Karagaiah P, Sonthalia S, et al. Selective RAR agonists for acne vulgaris: a narrative review［J］. J Cosmet Dermatol, 2020,19（6）:1278⁃1283. doi: 10.1111/jocd.13340.
［24］	Gericke J, Ittensohn J, Mihály J, et al. Regulation of retinoid⁃mediated signaling involved in skin homeostasis by RAR and RXR agonists/antagonists in mouse skin［J］. PLoS One, 2013,8（4）:e62643. doi: 10.1371/journal.pone.0062643.
［25］	Blume⁃Peytavi U, Fowler J, Kemény L, et al. Long⁃term safety and efficacy of trifarotene 50 μg/g cream, a first⁃in⁃class RAR⁃γ selective topical retinoid, in patients with moderate facial and truncal acne［J］. J Eur Acad Dermatol Venereol, 2020,34（1）:166⁃173. doi: 10.1111/jdv.15794.
［26］	Kim JM, Choo JE, Lee HJ, et al. Epidermal growth factor attenuated the expression of inflammatory cytokines in human epidermal keratinocyte exposed to Propionibacterium acnes［J］. Ann Dermatol, 2018,30（1）:54⁃63. doi: 10.5021/ad.2018.30.1.54.
［27］	Lichtenberger BM, Gerber PA, Holcmann M, et al. Epidermal EGFR controls cutaneous host defense and prevents inflammation［J］. Sci Transl Med, 2013,5（199）:199ra111. doi: 10.1126/scitranslmed.3005886.
［28］	Kim HK, Yeo IK, Li K, et al. Topical epidermal growth factor for the improvement of acne lesions: a randomized, double⁃blinded, placebo⁃controlled, split⁃face trial［J］. Int J Dermatol, 2014,53（8）:1031⁃1036. doi: 10.1111/ijd.12488.
［29］	Aydingoz IE, Tukenmez Demirci G, Agirbasli D, et al. The investigation of the amounts and expressions of epidermal growth factor, epidermal growth factor receptor, and epidermal growth factor receptor gene polymorphisms in acne vulgaris［J］. J Cosmet Dermatol, 2021,20（1）:346⁃351. doi: 10.1111/jocd.13498.
［30］	谷廷敏, 孙志刚, 牛星焘, 等. 创面愈合过程中表皮生长因子及其受体变化的临床研究［J］. 中华烧伤杂志, 2001,17（1）:52⁃53. doi: 10.3760/cma.j.issn.1009⁃2587.2001.01.016.
［31］	Gupta M, Mahajan VK, Mehta KS, et al. Peroxisome proliferator⁃activated receptors （PPARs） and PPAR agonists: the ′future′ in dermatology therapeutics?［J］. Arch Dermatol Res, 2015,307（9）:767⁃780. doi: 10.1007/s00403⁃015⁃1571⁃1.
［32］	Dozsa A, Mihaly J, Dezso B, et al. Decreased peroxisome proliferator⁃activated receptor γ level and signalling in sebaceous glands of patients with acne vulgaris［J］. Clin Exp Dermatol, 2016,41（5）:547⁃551. doi: 10.1111/ced.12794.
［33］	Elmongy NN, Shaker O. Expression of peroxisome proliferator activator receptor β/δ （PPARβ/δ） in acne vulgaris［J］. Eur J Dermatol, 2012,22（1）:42⁃45. doi: 10.1684/ejd.2011.1575.
［34］	Amr K, Abdel⁃Hameed M, Sayed K, et al. The Pro12Ala polymorphism of the gene for peroxisome proliferator activated receptor⁃gamma is associated with a lower Global Acne Grading System score in patients with acne vulgaris［J］. Clin Exp Dermatol, 2014,39（6）:741⁃745. doi: 10.1111/ced.12394.
［35］	Saeidi S, Chamaie⁃Nejad F, Ebrahimi A, et al. PPARγ Pro12Ala and C161T polymorphisms in patients with acne vulgaris: contribution to lipid and lipoprotein profile［J］. Adv Med Sci, 2018,63（1）:147⁃151. doi: 10.1016/j.advms.2017.09.003.
［36］	Shi G, Liao PY, Cai XL, et al. FoxO1 enhances differentiation and apoptosis in human primary keratinocytes［J］. Exp Dermatol, 2018,27（11）:1254⁃1260. doi: 10.1111/exd.13775.

[1]	宗杨永怡马楚君苏忠兰. 银屑病生物制剂治疗后湿疹化发生机制及应对策略[J]. 中华皮肤科杂志, 2024, 0(3): 20220578-e20220578.
[2]	刘亭微孟潇琦顾多多潘婼芯张悦许阳. 玫瑰痤疮发病机制的研究进展[J]. 中华皮肤科杂志, 2024, 57(2): 186-190.
[3]	古丽孜巴·图尔荪屈园园. Janus激酶-信号转导及转录激活因子信号通路抑制剂在白癜风治疗中的新进展[J]. 中华皮肤科杂志, 2024, 57(1): 71-75.
[4]	马晶晶亢盼郭森坚哲李春英李舒丽. 转录因子TFAP2B在健康人及白癜风患者表皮黑色素细胞中的表达模式[J]. 中华皮肤科杂志, 2024, 57(1): 29-33.
[5]	付丹丹李佳林付修宇张芯育胡华宋向凤田中伟. S100A10蛋白在银屑病皮损的表达及对小鼠银屑病样皮炎模型的影响[J]. 中华皮肤科杂志, 2023, 56(9): 839-844.
[6]	钟洁敏邵蕾梁毅敏黄琼霄夏曼琪刘玉梅. 射频火针与光动力疗法治疗面部中重度痤疮炎性皮损的疗效与安全性对比研究[J]. 中华皮肤科杂志, 2023, 56(8): 751-755.
[7]	张俐施健葛鑫刘念念陈赛张冬梅缪旭. Brahma相关基因1与激活转录因子2相互作用对皮肤鳞状细胞癌细胞增殖、迁移和侵袭能力的影响[J]. 中华皮肤科杂志, 2023, 56(8): 724-736.
[8]	宋志强陈奇权葛兰. 从特应性皮炎发病机制谈靶向治疗进展[J]. 中华皮肤科杂志, 2023, 56(8): 718-723.
[9]	唐志铭荆梦晴陆鹭单霄张翠侠张晓宇孟飒. 犀地凉血方通过LncRNA NEAT1/miR-485-5p/ STAT3调控网络对HaCaT细胞增殖、凋亡影响的研究[J]. 中华皮肤科杂志, 2023, 56(7): 642-650.
[10]	梁云生黎展宏伍奕蓓. [开放获取] 从发病机制认知变化看慢性自发性荨麻疹治疗进展[J]. 中华皮肤科杂志, 2023, 56(6): 552-558.
[11]	李嘉祺叶枫鞠强. 表皮葡萄球菌共生性稳态与皮肤疾病[J]. 中华皮肤科杂志, 2023, 56(5): 459-462.
[12]	郭伟楠王俊霞陈慧郝军峰李冰卫静宜赵涛. 自体脂肪干细胞胶填充治疗凹陷性痤疮瘢痕疗效观察[J]. 中华皮肤科杂志, 2023, 0(3): 20210867-e20210867.
[13]	杨剑秋刘倩楠周生儒李敏. 化脓性关节炎、坏疽性脓皮病、痤疮综合征1例并文献回顾[J]. 中华皮肤科杂志, 2023, 0(3): 20230253-e0230253.
[14]	张红燕李丽王明霞董银卯孟宏易帆. 益生菌在痤疮治疗中的应用进展[J]. 中华皮肤科杂志, 2023, 56(3): 283-285.
[15]	何谐栗玉珍. 靶向JAK-STAT信号通路治疗银屑病的研究进展[J]. 中华皮肤科杂志, 2023, 56(3): 273-278.

转录因子和受体调控痤疮发病机制的研究进展

Regulatory roles of transcription factors and receptors in the pathogenesis of acne

PDF

PDF (Mobile)

可视化

摘要/Abstract

引用本文

使用本文

参考文献 36

相关文章 15

Metrics

本文评价

推荐阅读 10