[1] |
Two AM, Wu W, Gallo RL, et al. Rosacea: part I. Introduction, categorization, histology, pathogenesis, and risk factors[J]. J Am Acad Dermatol, 2015,72(5):749⁃760. doi: 10.1016/j.jaad.2014.08. 028.<br />
|
[2] |
Woo YR, Lim JH, Cho DH, et al. Rosacea: molecular mechanisms and management of a chronic cutaneous inflammatory condition[J]. Int J Mol Sci, 2016,17(9):e1562. doi: 10.3390/ijms17091562.<br />
|
[3] |
Yamasaki K, Di NA, Bardan A, et al. Increased serine protease activity and cathelicidin promotes skin inflammation in rosacea[J]. Nat Med, 2007,13(8):975⁃980. doi: 10.1038/nm1616.<br />
|
[4] |
Bevins CL, Liu FT. Rosacea: skin innate immunity gone awry?[J]. Nat Med, 2007,13(8):904⁃906. doi: 10.1038/nm0807⁃904.<br />
|
[5] |
王岚琦, 鞠强. 玫瑰痤疮发生的免疫学研究进展[J]. 中华皮肤科杂志, 2017,50(3):219⁃221. doi: 10.3760/cma.j.issn.0412⁃4030. 2017.03.018.<br />
|
[6] |
Melnik BC. Rosacea: the blessing of the celts ⁃ an approach to patho⁃genesis through translational research[J]. Acta Derm Venereol, 2016,96(2):147⁃156. doi: 10.2340/00015555⁃2220.<br />
|
[7] |
Park K, Elias PM, Oda Y, et al. Regulation of cathelicidin anti⁃microbial peptide by an endoplasmic reticulum (ER) stress signaling, vitamin D receptor⁃independent pathway[J]. J Biol Chem, 2011,286(39):34121⁃34130. doi: 10.1074/jbc.M111. 250431.<br />
|
[8] |
Melnik BC. Endoplasmic reticulum stress: key promoter of rosacea pathogenesis[J]. Exp Dermatol, 2014,23(12):868⁃873. doi: 10.1111/ exd.12517.<br />
|
[9] |
Yamasaki K, Kanada K, Macleod DT, et al. TLR2 is increased in rosacea and stimulates enhanced serine protease production by keratinocytes[J]. J Invest Dermatol, 2011,131(3):688⁃697. doi: 10.1038/jid.2010.351.<br />
|
[10] |
Yamasaki K, Schauber J, Coda A, et al. Kallikrein⁃mediated proteolysis regulates the antimicrobial effects of cathelicidins in skin[J]. FASEB J, 2006,20(12):2068⁃2080. doi: 10.1096/fj.06⁃6075com.<br />
|
[11] |
Antal AS, Dombrowski Y, Koglin S, et al. Impact of vitamin D3 on cutaneous immunity and antimicrobial peptide [J]. Dermatoendocrinol, 2011,3(1):18⁃22. doi: 10.4161/derm.3.1. 14616.<br />
|
[12] |
Morizane S, Yamasaki K, Kabigting FD, et al. Kallikrein ex⁃pression and cathelicidin processing are independently controlled in keratinocytes by calcium, vitamin D(3), and retinoic acid[J]. J Invest Dermatol, 2010,130(5):1297⁃1306. doi: 10.1038/jid.2009. 435.<br />
|
[13] |
Korting HC, Schöllmann C. Tetracycline actions relevant to rosacea treatment[J]. Skin Pharmacol Physiol, 2009,22(6):287⁃294. doi: 10.1159/000235550.<br />
|
[14] |
Kanada KN, Nakatsuji T, Gallo RL. Doxycycline indirectly inhibits proteolytic activation of tryptic kallikrein⁃related peptidases and activation of cathelicidin[J]. J Invest Dermatol, 2012,132(5):1435⁃1442. doi: 10.1038/jid.2012.14.<br />
|
[15] |
Tjabringa GS, Aarbiou J, Ninaber DK, et al. The antimicrobial peptide LL⁃37 activates innate immunity at the airway epithelial surface by transactivation of the epidermal growth factor receptor[J]. J Immunol, 2003,171(12):6690⁃6696.<br />
|
[16] |
Tokumaru S, Sayama K, Shirakata Y, et al. Induction of kera⁃tinocyte migration via transactivation of the epidermal growth factor receptor by the antimicrobial peptide LL⁃37[J]. J Immunol, 2005,175(7):4662⁃4668.<br />
|
[17] |
Mascarenhas NL, Wang Z, Chang YL, et al. TRPV4 mediates mast cell activation in cathelicidin⁃induced rosacea inflammation[J]. J Invest Dermatol, 2017,137(4):972⁃975. doi: 10.1016/j.jid. 2016.10.046.<br />
|
[18] |
Salzer S, Kresse S, Hirai Y, et al. Cathelicidin peptide LL⁃37 increases UVB⁃triggered inflammasome activation: possible implications for rosacea[J]. J Dermatol Sci, 2014,76(3):173⁃179. doi: 10.1016/j.jdermsci.2014.09.002.<br />
|
[19] |
Filewod NC, Pistolic J, Hancock RE. Low concentrations of LL⁃37 alter IL⁃8 production by keratinocytes and bronchial epithelial cells in response to proinflammatory stimuli[J]. FEMS Immunol Med Microbiol, 2009,56(3):233⁃240. doi: 10.1111/j.1574⁃695X. 2009.00571.x.<br />
|
[20] |
Coda AB, Hata T, Miller J, et al. Cathelicidin, kallikrein 5, and serine protease activity is inhibited during treatment of rosacea with azelaic acid 15 gel[J]. J Am Acad Dermatol, 2013,69(4):570⁃577. doi: 10.1016/j.jaad.2013.05.019.<br />
|
[21] |
Liu PT, Krutzik SR, Kim J, et al. Cutting edge: all⁃trans retinoic acid down⁃regulates TLR2 and function[J]. J Immunol, 2005,174(5):2467⁃2470.<br />
|
[22] |
Chang AL, Alora⁃Palli M, Lima XT, et al. A randomized, double⁃blind, placebo⁃controlled, pilot study to assess the efficacy and safety of clindamycin 1.2 and tretinoin 0.025 combination gel for the treatment of acne rosacea over 12 weeks[J]. J Drugs Dermatol, 2012,11(3):333⁃339.<br />
|
[23] |
de Ménonville ST, Rosignoli C, Soares E, et al. Topical treatment of rosacea with ivermectin inhibits gene of cathelicidin innate immune mediators, LL⁃37 and KLK5, in reconstructed and ex vivo skin models[J]. Dermatol Ther (Heidelb), 2017,7(2):213⁃225. doi: 10.1007/s13555⁃017⁃0176⁃3.<br />
|
[24] |
Moran EM, Foley R, Powell FC. Demodex and rosacea revisited[J]. Clin Dermatol, 2017,35(2):195⁃200. doi: 10.1016/j.clindermatol. 2016.10.014.<br />
|
[25] |
Lee JB, Bae SH, Moon KR, et al. Light⁃emitting diodes down⁃regulate cathelicidin, kallikrein and toll⁃like receptor 2 expres⁃sions in keratinocytes and rosacea⁃like mouse skin[J]. Exp Dermatol, 2016,25(12):956⁃961. doi: 10.1111/exd.13133.<br />
|