[1] Kageyama Y, Aida K, Kawauchi K, et al. Higher incidence of zinc and nickel hypersensitivity in patients with irritable bowel syndrome[J]. Immun Inflamm Dis, 2019, 7:304-307. [2] Baj A, Bistoletti M, Bosi A, et al. Marine toxins and nociception: potential therapeutic use in the treatment of visceral pain associated with gastrointestinal disorders[J]. Toxins, 2019, 11:1-37. [3] Chalazonitis A, Rao M. Enteric nervous system manifestations of neurodegenerative disease[J]. Brain Res, 2018, 1693:207-213. [4] Nagy N, Goldstein AM. Enteric nervous system development: a crest cell's journey from neural tube to colon[J]. Semin Cell Dev Biol, 2017, 66:94-106. [5] Cryan JF, O'Riordan KJ, Cowan C, et al. The microbiota-gut-brain axis[J]. Physiol Rev, 2019, 99:1877-2013. [6] Scanzi J, Accarie A, Muller E, et al. Colonic overexpression of the T-type calcium channel Cav 3.2 in a mouse model of visceral hypersensitivity and in irritable bowel syndrome patients[J]. Neurogastroenterol Motil, 2016, 28: 1632-1640. [7] Hull JM, Isom LL. Voltage-gated sodium channel β subunits: the power outside the pore in brain development and disease[J]. europharmacology, 2018, 132:43-57. [8] 郭子涵, 赵正, 刘晓, 等. 离子通道与肠易激综合征发病机制的研究进展[J]. 胃肠病学, 2019, 24:501-504. [9] Saito YA, Strege PR, Tester DJ, et al. Sodium channel mutation in irritable bowel syndrome: evidence for an ion channelopathy[J]. Am J Physiol Gastrointest Liver Physiol, 2009, 296:G211-G218. [10] Strege PR, Mazzone A, Bernard CE, et al. Irritable bowel syndrome patients have SCN5A channelopathies that lead to decreased NaV1.5 current and mechanosensitivity[J]. Am J Physiol Gastrointest Liver Physiol, 2018, 314:G494-G503. [11] Zamponi GW, Striessnig J, Koschak A, et al. The physiology, pathology, and pharmacology of voltage-gated calcium channels and their future therapeutic potential[J]. Pharmacol Rev, 2015, 67:821-870. [12] Gadotti VM, Zamponi GW. Disrupting USP5/Cav3.2 interactions protects female mice from mechanical hypersensitivity during peripheral inflammation[J]. Mol Brain, 2018, 11:60-62. [13] Zhu J, Luo HS, Chen L, et al. Altered expression of L-type calcium channel alpha1C and alpha1D subunits in colon of rats with diarrhea-predominant irritable bowel syndrome[J]. CMJ, 2009, 89:2713-2717. [14] Qian A, Song D, Li Y, et al. Role of voltage gated Ca2+ channels in rat visceral hypersensitivity change induced by 2,4,6-trinitrobenzene sulfonic acid[J]. Mol Pain, 2013, 9:15-24. [15] Picard E, Carvalho FA, Agosti F, et al. Inhibition of Cav 3.2 calcium channels: a new target for colonic hypersensitivity associated with low-grade inflammation[J]. Br J Pharmacol, 2019, 176:950-963. [16] Balemans D, Boeckxstaens GE, Talavera K, et al. Transient receptor potential ion channel function in sensory transduction and cellular signaling cascades underlying visceral hypersensitivity[J]. Am J Physiol Gastrointest Liver Physiol, 2017, 312:G635-G648. [17] Csekö K, Beckers B, Keszthelyi D, et al. Role of TRPV1 and TRPA1 ion channels in inflammatory bowel diseases: potential therapeutic targets?[J]. Pharmaceuticals, 2019, 12:48-66. [18] Zhou Q, Yang L, Larson S, et al. Decreased miR-199 augments visceral pain in patients with IBS through translational upregulation of TRPV1[J]. Gut, 2016, 65:797-805. [19] Xu XJ, Zhang YL, Liu L, et al. Increased expression of nerve growth factor correlates with visceral hypersensitivity and impaired gut barrier function in diarrhoea-predominant irritable bowel syndrome: a preliminary explorative study[J]. Aliment Pharmacol Ther, 2017, 45:100-114. [20] Beckers AB, Weerts Z, Helyes Z, et al. Review article: transient receptor potential channels as possible therapeutic targets in irritable bowel syndrome[J]. Aliment Pharmacol Ther, 2017, 46:938-952. [21] Balemans D, Aguilera-Lizarraga J, Florens MV, et al. Histamine-mediated potentiation of transient receptor potential (TRP) ankyrin 1 and TRP vanilloid 4 signaling in submucosal neurons in patients with irritable bowel syndrome[J]. Am J Physiol Gastrointest Liver Physiol, 2019, 316: G338-G349. [22] de Jong PR, Takahashi N, Peiris M, et al. TRPM8 on mucosal sensory nerves regulates colitogenic responses by innate immune cells via GRP[J]. Mucosal Immunol, 2015, 8: 491-504. [23] Henström M, Hadizadeh F, Beyder A, et al. TRPM8 polymorphisms associated with increased risk of IBS-C and IBS-M[J]. Gut, 2017, 66: 1725-1727. |