[1]张晶晶,CHEN Jun-hao,赵美平,等.内质网应激在大鼠低氧高二氧化碳性肺动脉高压中的作用[J].中国应用生理学杂志,2018,4:327-333+387. [2]Aierken A, Li MY, Li Q, et al. 4-phenylbutyric acid induces protection against pulmonary arterial hypertension in rats[J]. PLoS One, 2016, 11:e0157538. doi: 10.1371/journal.pone.0157538. [3]Wu J, Pan W, Wang C, et al. H2S attenuates endo-plasmic reticulum stress in hypoxia-induced pulmonary artery hypertension[J]. Biosci Rep, 2019, 39:BSR20190304. doi: 10.1042/BSR20190304. [4]Chen R, Zhong W, Shao C, et al. Docosahexaenoic acid inhibits monocrotaline-induced pulmonary hypertension via attenuating endoplasmic reticulum stress and inflammation[J]. Am J Physiol Lung Cell Mol Physiol, 2018, 314:L243-L255. [5]范小芳,李文娟,陈兆琴,等.慢性低氧性肺动脉高压大鼠肺组织内质网应激介导的凋亡的变化[J].中国应用生理学杂志,2011,27: 270-274. [6]Naiel S, Tat V, Padwal M, et al. Protein misfolding and endoplasmic reticulum stress in chronic lung disease: will cell-specific targeting be the key to the cure[J]. Chest, 2020, 157:1207-1220. [7]Chen A, Liu J, Zhu J, et al. FGF21 attenuates hypoxia induced dysfunction and apoptosis in HPAECs through alleviating endoplasmic reticulum stress[J]. Int J Mol Med, 2018, 42:1684-1694. [8]Karali E, Bellou S, Stellas D, et al. VEGF signals through ATF6 and PERK to promote endothelial cell survival and angiogenesis in the absence of ER stress[J]. Mol Cell, 2014, 54:559-572. [9]Shanahan CM, Furmanik M. Endoplasmic reticulum stress in arterial smooth muscle cells: a novel regulator of vascular disease[J]. Curr Cardiol Rev, 2017, 13:94-105. [10]Teng RJ, Rana U, Afolayan AJ, et al. Nogo-B receptor modulates angiogenesis response of pulmonary artery endothelial cells through eNOS coupling[J]. Am J Respir Cell Mol Biol, 2014, 51:169-177. [11]Ying R, Wang XQ, Yang Y, et al. Hydrogen sulfide suppresses endoplasmic reticulum stress-induced endothelial-to-mesenchymal transition through Src pathway[J]. Life Sci, 2016, 144:208-217. [12]Good RB, Gilbane AJ, Trinder SL, et al. Endothelial to mesenchymal transition contributes to endothelial dysfunction in pulmonary arterial hypertension[J]. Am J Pathol, 2015,185:1850-1858. [13]Yeager ME, Belchenko DD, Nguyen CM, et al. Endothelin-1, the unfolded protein response, and persistent inflammation: role of pulmonary artery smooth muscle cells[J]. Am J Respir Cell Mol Biol, 2012, 46:14-22. [14]Koyama M, Furuhashi M, Ishimura S, et al. Reduction of endoplasmic reticulum stress by 4-phenylbutyric acid prevents the development of hypoxia-induced pulmonary arterial hypertension[J]. Am J Physiol Heart Circ Physiol. Heart and circulatory physiology, 2014, 306:H1314-H1323. [15]Sutendra G, Dromparis P, Wright P, et al. The role of Nogo and the mitochondria-endoplasmic reticulum unit in pulmonary hypertension[J]. Sci Transl Med, 2011, 3:55r-88r. [16]Dromparis P, Paulin R, Stenson TH, et al. Attenuating endoplasmic reticulum stress as a novel therapeutic strategy in pulmonary hypertension[J]. Circulation, 2013, 127:115-125. [17]Yang YD, Li MM, Xu G, et al. Nogo-B receptor directs mitochondria-associated membranes to regulate vascular smooth muscle cell proliferation[J]. Int J Mol Sci, 2019, 20:2319. doi: 10.3390/ijms20092319. [18]Shimizu T, Higashijima Y, Kanki Y, et al. PERK inhibition attenuates vascular remodeling in pulmonary arterial hypertension caused by BMPR2 mutation[J]. Sci Signal, 2021, 14:eabb 3616. doi: 10.1126/scisignal.abb3616. [19]Wang AP, Li XH, Yang YM, et al. A critical role of the mTOR/eIF2α pathway in hypoxia-induced pulmonary hypertension[J]. PLoS One, 2015, 10:e0130806.doi: 10.1371/journal.pone.0130806. [20]Shi Z, Xu L, Xie H, et al. Attenuation of intermittent hypoxia-induced apoptosis and fibrosis in pulmonary tissues via suppression of ER stress activation[J]. BMC Pulm Med, 2020, 20:92. doi: 10.1186/s12890-020-1123-0. [21]Jiang H, Niu Y, He Y, et al. Proteomic analysis reveals that XBP1s promotes hypoxic pulmonary hypertension through the p-JNK MAPK pathway[J]. J Cell Physiol, 2022, 237:1948-1963. [22]Cao X, He Y, Li X, et al. The IRE1α-XBP1 pathway function in hypoxia-induced pulmonary vascular remodel-ing, is upregulated by quercetin, inhibits apoptosis and partially reverses the effect of quercetin in PASMCs[J]. Am J Transl Res, 2019, 11:641-654. [23]Wang F, Xu X, Tang W, et al.Rab6A GTPase contri-butes to phenotypic modulation in pulmonary artery smooth muscle cells under hypoxia[J]. J Cell Biochem, 2018.10.1002/jcb.28060. doi: 10.1002/jcb.28060. [24]李圣维,夏国际,熊墨煌,等.内质网应激促进肺动脉平滑肌细胞的表型转化[J]. 现代生物医学进展,2018,3:458-462. [25]唐为安,王芳,杨俊俊,等.ATF6基因对低氧状态下肺动脉平滑肌表型转化的调控作用[J]. 中国细胞生物学学报,2018,40: 1285-1294. |