[1]罗芩 何庆.TNF凝集素样结构域：高原肺水肿药物治疗新选择罗芩 何庆2[J].心血管病学进展,2019,(9):1301-1304.[doi:10.16806/j.cnki.issn.1004-3934.2019.00.030]
　LUO QinHE Qing.The Lectin-like Domain of TNF:New Drug Treatment Option for HAPE[J].Advances in Cardiovascular Diseases,2019,(9):1301-1304.[doi:10.16806/j.cnki.issn.1004-3934.2019.00.030]
点击复制

TNF凝集素样结构域：高原肺水肿药物治疗新选择罗芩 何庆2()
分享到：

《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2019年9期
页码:
1301-1304
栏目:
综述
出版日期:
2019-12-25

文章信息/Info

Title:
The Lectin-like Domain of TNF:New Drug Treatment Option for HAPE
作者:
罗芩1 何庆2
( 1．西南交通大学医学院,四川 成都 610036 ;2．西南交通大学医学院 西南交通大学附属医院 成都市第三人民医院,四川 成都 610036)
Author(s):
LUO Qin1HE Qing2
(1. Southwest Jiaotong University College of Medcine, Chengdu 610036, Sichuan, China;2.Southwest Jiaotong University College of Medcine, The Affiliated Hospital of Southwest Jiaotong University, The Third People’s Hospital of Chengdu, Chengdu 610036, Sichuan, China)
关键词:
高原肺水肿; TNF凝集素样结构域; 药物治疗
Keywords:
High altitude pulmonary edema; The lectin-like domain of TNF; Pharmacotherapy
DOI:
10.16806/j.cnki.issn.1004-3934.2019.00.030
摘要:
高原肺水肿是高原地区人群常见的高原疾病之一，严重威胁着人们的生命健康。它的发病机制目前尚未完全清楚，主要与驱动水进入肺泡的力量和清除肺泡液的能力两者失衡有关。目前用于治疗高原肺水肿的药物大多作用机制不明且不良反应较多。而TNF凝集素样结构域一方面能直接激活Ⅱ型肺泡上皮顶端钠通道，加速水肿肺的肺泡液清除；另一方面还具有抗炎作用，能减慢肺水肿的形成，是高原肺水肿药物治疗的一种新选择。
Abstract:
High altitude pulmonary edema is one of the common diseases in high altitude area, which seriously threatens people’s life and health. Its pathogenesis is still not fully understood and is related to an imbalance between the force that drives water into the alveoli and the ability to clear alveolar fluid. At present, most drugs used to treat high altitude pulmonary edema have an unclear mechanism of action and many adverse reactions. The lectin-like domain of TNF on the one hand can directly activate type Ⅱ alveolar epithelial sodium channel to accelerate the clearance of alveolar fluid; and on the other hand, it has anti-inflammatory effect and can slow down the formation of pulmonary edema. So, the lectin-like domain of TNF is a new option for the pharmacotherapy of high-altitude pulmonary edema

参考文献/References:

[1] Hackett PH, Roach RC. High-altitude illness[J]. N Engl J Med,2001,345(2):107-114.

[2] Wilkins MR, Ghofrani HA, Weissmann N, et al. Pathophysiology and treatment of high-altitude pulmonary vascular disease[J]. Circulation, 2015, 131(6):582-590.

[3] Wu TY, Ding SQ, Liu JL, et al. Who should not go high: chronic disease and work at altitude during construction of the Qinghai-Tibet railroad[J]. High Alt Med Biol,2007,8(2):88-107.

[4] Maggiorini M. Prevention and treatment of high-altitude pulmonary edema[J]. Prog Cardiovasc Dis, 2010,52(6):500-506.

[5] Bartsch P, Mairbaurl H, Maggiorini M, et al. Physiological aspects of high-altitude pulmonary edema[J]. J Appl Physiol (1985), 2005, 98(3): 1101-1110.

[6] Basnyat B, Murdoch DR. High-altitude illness[J]. Lancet, 2003, 361(9373): 1967-1974.

[7] Scherrer U, Rexhaj E, Jayet PY, et al. New insights in the pathogenesis of high-altitude pulmonary edema[J]. Prog Cardiovasc Dis,2010,52(6):485-492.

[8] 谭秀娟,何庆.高原肺动脉高压发病机制研究进展[J].心血管病学进展,2018,39(04):674-677.

[9] Joyce KE, Lucas SJE, Imray CHE, et al. Advances in the available non-biological pharmacotherapy prevention and treatment of acute mountain sickness and high altitude cerebral and pulmonary oedema[J]. Expert Opin Pharmacother,2018,19(17):1891-1902.

[10] Luks AM, Swenson ER, Bartsch P. Acute high-altitude sickness[J]. Eur Respir Rev, 2017, 26(143).?pii: 160096. doi: 10.1183/16000617.0096-2016.

[11] Hummler E, Barker P, Gatzy J, et al. Early death due to defective neonatal lung liquid clearance in alpha-ENaC-deficient mice[J]. Nat Genet, 1996, 12(3): 325-328.

[12] Gille T, Randrianarison-Pellan N, Goolaerts A, et al. Hypoxia-induced inhibition of epithelial Na(+) channels in the lung. Role of Nedd4-2 and the ubiquitin-proteasome pathway[J]. Am J Respir Cell Mol Biol, 2014, 50(3):526-537.

[13] Urner M, Herrmann IK, Booy C, et al. Effect of hypoxia and dexamethasone on inflammation and ion transporter function in pulmonary cells[J]. Clin Exp Immunol, 2012, 169(2): 119-128.

[14] Luks AM, Auerbach PS, Freer L, et al. Wilderness medical society practice guidelines for the prevention and treatment of acute altitude illness: 2019 update[J]. Wilderness Environ Med, 2019 Jun 24. pii: S1080-6032(19)30090-0. doi: 10.1016/j.wem.2019.04.006.

[15] Li Y, Zhang Y, Zhang Y. Research advances in pathogenesis and prophylactic measures of acute high altitude illness[J]. Respir Med, 2018, 145: 145-152.

[16] Hazemi P, Tzotzos SJ, Fischer B, et al. Essential structural features of TNF-alpha lectin-like domain derived peptides for activation of amiloride-sensitive sodium current in A549 cells[J]. J Med Chem,2010,53(22):8021-8029.

[17] Shabbir W, Scherbaum-Hazemi P, Tzotzos S, et al. Mechanism of action of novel lung edema therapeutic AP301 by activation of the epithelial sodium channel[J]. Mol Pharmacol,2013,84(6): 899-910.

[18] Lucas R, Yue Q, Alli A, et al. The lectin-like domain of TNF increases ENaC open probability through a novel site at the interface between the second transmembrane and C-terminal domains of the alpha-subunit[J]. J Biol Chem,2016, 291(45): 23440-23451.

[19] Shabbir W, Tzotzos S, Bedak M, et al. Glycosylation-dependent activation of epithelial sodium channel by solnatide[J]. Biochem Pharmacol, 2015, 98(4): 740-753.

[20] Alli AA, Bao HF, Alli A A, et al. Phosphatidylinositol phosphate-dependent regulation of Xenopus ENaC by MARCKS protein[J]. Am J Physiol Renal Physiol, 2012, 303(6): F800-F811.

[21] Czikora I, Alli A, Bao HF, et al. A novel tumor necrosis factor-mediated mechanism of direct epithelial sodium channel activation[J]. Am J Respir Crit Care Med, 2014, 190(5): 522-532.

[22] Aigner C, Slama A, Barta M, et al. Treatment of primary graft dysfunction after lung transplantation with orally inhaled AP301: A prospective, randomized pilot study[J]. J Heart Lung Transplant, 2017 Sep 30.pii: S1053-2498(17)32036-3. doi: 10.1016/j.healun.2017.09.021.

[23] Krenn K, Lucas R, Croize A, et al. Inhaled AP301 for treatment of pulmonary edema in mechanically ventilated patients with acute respiratory distress syndrome: a phase Ⅱa randomized placebo-controlled trial[J]. Crit Care, 2017, 21(1): 194.

[24] Schwameis R, Eder S, Pietschmann H, et al. A FIM study to assess safety and exposure of inhaled single doses of AP301-A specific ENaC channel activator for the treatment of acute lung injury[J]. J Clin Pharmacol, 2014, 54(3): 341-350.

[25] Madaio MP, Czikora I, Kvirkvelia N, et al. The TNF-derived TIP peptide activates the epithelial sodium channel and ameliorates experimental nephrotoxic serum nephritis[J]. Kidney Int, 2019,95(6):1359-1372.

[26] Zhou Q, Wang D, Liu Y, et al. Solnatide demonstrates profound therapeutic activity in a rat model of pulmonary edema induced by acute hypobaric hypoxia and exercise[J]. Chest,2017,151(3): 658-667.

相似文献/References:

[1]罗芩 何庆?/html>.腺苷2B受体激动剂对大鼠高原肺水肿的治疗作用[J].心血管病学进展,2021,(10):941.[doi:10.16806/j.cnki.issn.1004-3934.2021.10.019]
　LUO Qin,HE Qing.Therapeutic Effect of Adenosine 2B Receptor Agonist on High-Altitude Pulmonary Edema in Rats[J].Advances in Cardiovascular Diseases,2021,(9):941.[doi:10.16806/j.cnki.issn.1004-3934.2021.10.019]

更新日期/Last Update: 2020-02-06