参考文献/References:
[1]GIUDICE L CClinical practice.Endometriosis [J]. New England Journal of Medicine, 2010, 362 (25) : 2389-2398.
[2]中华医学会妇产科学分会子宫内膜异位症协作组.子宫内膜异位症的诊治指南 [J].中华妇产科杂志,2015,50(3):161-169.
[3]RUIZ A, ROCKFIELD S, TARAN N, et al. Effect of hydroxychloroquine and characterization of autophagy in a mouse model of endometriosis [J]. Cell Death & Disease, 2016, 7(1): e2059-e2077.
[4]TAYLOR R N, YU Jie, TORRES P B, et al. Mechanistic and therapeutic implications of angiogenesis in endometriosis [J]. Reproductive Sciences, 2009, 16 (2) : 140-146.
[5]SANTULLI P, MARCELLIN L, TOSTI C, et al. MAP kinases and the inflammatory signaling cascade as targets for the treatment of endometriosis [J]. Expert Opinion on Therapeutic Targets, 2015, 19 (11) : 1465-1483.
[6]BROWNE A S, YU Jie, HUANG Ruo-pan, et al. Proteomic identification of neurotrophins in the eutopic endometrium of women with endometriosis [J]. Fertility and Sterility, 2012, 98 (3): 713-719.
[7]Borghese B, Vaiman D, Mondon F, et al.Neurotrophins and pain in endometriosis [J]. Gynecol Obstet Fertil,2010,38 (7-8) : 442-446.
[8]ANGER D L, ZHANG Bingjun, BOUTROSS-TADROSS O, et al. Tyrosine receptor kinase B (TrkB) protein expression in the human endometrium [J]. Endocrine, 2007, 31 (2) : 167-173.
[9]DEWANTO A, DUDAS J, GLUECKERT R, et al. Localization of TrkB and p75 receptors in peritoneal and deep infiltrating endometriosis: an immunohistochemical study [J]. Reproductive Biology and Endocrinology : RB&E, 2016, 14 (1): 43.
[10]YU Xiao-hui, LIU Ling, CAI Bin, et al. Suppression of anoikis by the neurotrophic receptor TrkB in human ovarian cancer [J]. Cancer Science, 2008, 99 (3): 543-552.
[11]BAI Huimin, LI Haixia, LI Weihua, et al. The PI3K/AKT/mTOR pathway is a potential predictor of distinct invasive and migratory capacities in human ovarian cancer cell lines [J]. Oncotarget, 2015, 6 (28): 25520-25532.
[12]LECONTE M, NICCO C, NG C, et al. The mTOR/AKT inhibitor temsirolimus prevents deep infiltrating endometriosis in mice [J]. The American Journal of Pathology, 2011, 179 (2) : 880-889.
[13]SMITH E D, PRIETO G A, TONG Liqi, et al. Rapamycin and interleukin-1β impair brain-derived neurotrophic factor-dependent neuron survival by modulating autophagy [J]. The Journal of Biological Chemistry, 2014, 289 (30): 20615-20629.
[14]LEE I I, KIM J J. Influence of AKT on progesterone action in endometrial diseases [J]. Biology of Reproduction, 2014, 91(3): 63.
[15]KIM T H, YU Yanni, LUO L, et al. Activated AKT pathway promotes establishment of endometriosis [J]. Endocrinology, 2014, 155 (5): 1921-1930.
[16]EATON J L, UNNO K, CARAVEO M, et al. Increased AKT or MEK1/2 activity influences progesterone receptor levels and localization in endometriosis [J]. The Journal of Clinical Endocrinology and Metabolism, 2013, 98 (12): E1871-E1879.
[17]BLAIS M, LVESQUE P, BELLENFANT S, et al. Nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3 and glial-derived neurotrophic factor enhance angiogenesis in a tissue-engineered in vitro model [J]. Tissue Engineering Part a, 2013, 19 (15/16): 1655-1664.
[18]USUI T, NARUO A, OKADA M, et al. Brain-derived neurotrophic factor promotes angiogenic tube formation through generation of oxidative stress in human vascular endothelial cells [J]. Acta Physiologica (Oxford, England), 2014, 211 (2): 385-394.
[19]HUANG Feng-ying, CAO Jing, LIU Qiu-hong, et al. MAPK/ERK signal pathway involved expression of COX-2 and VEGF by IL-1β induced in human endometriosis stromal cells in vitro [J]. International Journal of Clinical and Experimental Pathology, 2013, 6 (10): 2129-2136.
[20]CORDEIRO C A, VIEIRA E L, ROCHA N P, et al. Serum levels of neurotrophic factors in active toxoplasmic retinochoroiditis [J]. The Brazilian Journal of Infectious Diseases : an Official Publication of the Brazilian Society of Infectious Diseases, 2016,20 (12):30584-30590.
[21]BUROTTO M, CHIOU V L, LEE J M, et al. The MAPK pathway across different malignancies: a new perspective [J]. Cancer, 2014, 120 (22) : 3446-3456.
[22]BOUTAHAR N, REYNAUD E, LASSABLIERE F, et al. Brain-derived neurotrophic factor inhibits cell cycle reentry but not endoplasmic reticulum stress in cultured neurons following oxidative or excitotoxic stress [J]. Journal of Neuroscience Research, 2010, 88 (10): 2263-2271.
[23]CALABRESE F, ROSSETTI A C, RACAGNI G, et al. Brain-derived neurotrophic factor: a bridge between inflammation and neuroplasticity [J]. Frontiers in Cellular Neuroscience, 2014, 8 (12): 430-436.
[24]MOROTTI M, VINCENT K, BRAWN J, et al. Peripheral changes in endometriosis-associated pain [J]. Human Reproduction Update, 2014, 20 (5) : 717-736.
[25]CRUZ DUARTE P, ST-JACQUES B, MA Weiya. Prostaglandin E2 contributes to the synthesis of brain-derived neurotrophic factor in primary sensory neuron in ganglion explant cultures and in a neuropathic pain model [J]. Experimental Neurology, 2012, 234 (2) : 466-481.
[26]代淑红,马正良.钾氯共转运体-2和痛觉过敏关系的研究进展 [J].国际麻醉学与复苏杂志,2015,36 (6):543-546.
[27]GUPTA S, GHULMIYYAH J, SHARMA R, et al. Power of proteomics in linking oxidative stress and female infertility [J]. BioMed Research International, 2014 (2014): 916212-91638.
[28]DORFMAN M D, KERR B, GARCIA-RUDAZ C, et al. Neurotrophins acting via TRKB receptors activate the JAGGED1-NOTCH2 cell-cell communication pathway to facilitate early ovarian development [J]. Endocrinology, 2011, 152 (12): 5005-5016.
[29]BUYUK E, SEIFER D B. Follicular-fluid neurotrophin levels in women undergoing assisted reproductive technology for different etiologies of infertility [J]. Fertility and Sterility, 2008, 90 (5): 1611-1615.
[30]ZHANG Q-y, GUAN Q, WANG Y, et al. BDNF Val66Met polymorphism is associated with Stage III-IV endometriosis and poor in vitro fertilization outcome [J]. Human Reproduction (Oxford, England), 2012, 27 (6): 1668-1675.
[31]BARCENA DE ARELLANO M L, ARNOLD J, LANG H, et al. Evidence of neurotrophic events due to peritoneal endometriotic lesions [J]. Cytokine, 2013, 62 (2): 253-261.
[32]WESSELS J M, KAY V R, LEYLAND N A, et al. Assessing brain-derived neurotrophic factor as a novel clinical marker of endometriosis [J]. Fertility and Sterility, 2016, 105 (1): 119-128.e1.
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