内质网应激在低氧性肺动脉高压中作用的研究进展

doi:10.16352/j.issn.1001-6325.2023.05.0848

基础医学与临床 ›› 2023, Vol. 43 ›› Issue (5): 848-851.doi: 10.16352/j.issn.1001-6325.2023.05.0848

内质网应激在低氧性肺动脉高压中作用的研究进展

刘幸幸, 王威威^*, 袁好鑫

哈尔滨医科大学附属第二医院麻醉科,黑龙江哈尔滨 150086

收稿日期:2022-04-20 修回日期:2022-06-29 出版日期:2023-05-05 发布日期:2023-04-26
通讯作者: ^*wangweiwei_1980@126.com

Research progress of endoplasmic reticulum stress of hypoxic pulmonary hypertension

LIU Xingxing, WANG Weiwei^*, YUAN Haoxin

Department of Anesthesiology, the Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China

Received:2022-04-20 Revised:2022-06-29 Online:2023-05-05 Published:2023-04-26
Contact: ^*wangweiwei_1980@126.com

摘要/Abstract

摘要： 低氧性肺动脉高压(HPH)是长期低氧导致的血管持续性收缩和血管不可逆重塑的严重肺部并发症。低氧可干扰内质网腔内蛋白质折叠过程,激活内质网应激(ERS)。ERS作为细胞应激的核心反应,与HPH的发生发展关系密切。

关键词: 低氧性肺动脉高压, 内质网应激, 未折叠蛋白反应

Abstract: Hypoxic pulmonary hypertension (HPH) is a serious complication caused by long-term hypoxia,which is characterized by persistent vasoconstriction and irreversible vascular remodeling. The hypoxia may destroy protein folding process in endoplasmic reticulum and activate endoplasmic reticulum stress(ERS). As the core response of cell stress, ERS is closely related to the development of HPH.

Key words: hypoxic pulmonary hypertension, endoplasmic reticulum stress, unfolded protein response

中图分类号:

刘幸幸, 王威威, 袁好鑫. 内质网应激在低氧性肺动脉高压中作用的研究进展[J]. 基础医学与临床, 2023, 43(5): 848-851.

LIU Xingxing, WANG Weiwei, YUAN Haoxin. Research progress of endoplasmic reticulum stress of hypoxic pulmonary hypertension[J]. Basic & Clinical Medicine, 2023, 43(5): 848-851.

参考文献

[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.

内质网应激在低氧性肺动脉高压中作用的研究进展

Research progress of endoplasmic reticulum stress of hypoxic pulmonary hypertension

PDF

可视化

摘要/Abstract

引用本文

使用本文

参考文献

相关文章 15

编辑推荐

Metrics

本文评价

[1]	金涛, 杨青山, 吴树金, 朱晓燕, 史宇悰, 牛建雄, 刘林. 内质网应激在骨关节炎中作用的研究进展[J]. 基础医学与临床, 2023, 43(3): 476-480.
[2]	李明皓, 范亮亮, 项荣. 内质网应激在丙肝病毒感染发病学中作用的研究进展[J]. 基础医学与临床, 2022, 42(2): 316-320.
[3]	刘青, 张蕾, 张利元, 王世凤, 左立旻. Circ_0038467靶向miR-182调控肺炎链球菌(Sp)诱导的人肺泡上皮细胞系HPAEpiC损伤[J]. 基础医学与临床, 2021, 41(9): 1277-1284.
[4]	张志敏, 苟丽沙, 马丽群, 任可, 路军, 魏星, 李慧杰, 周圣华. 达格列净降低心力衰竭大鼠心肌内质网应激并缓解左室重构[J]. 基础医学与临床, 2021, 41(12): 1742-1748.
[5]	李招兵, 马小峰, 江振涛, 黄云辉. 烟酸姜黄素酯抑制LPS诱导的HUVECs分泌炎性细胞因子与内质网应激[J]. 基础医学与临床, 2021, 41(1): 62-67.
[6]	杨李莉, 郭志新, 冯劲宜, 宋英伦, 石文娇. 重组球形脂联素减轻糖尿病小鼠肾脏损伤[J]. 基础医学与临床, 2020, 40(4): 518-522.
[7]	董季罗乐宋振蓉李洁陈敏张轩萍. Nox1/4抑制剂减轻脂多糖致人脐静脉融合细胞的损伤[J]. 基础医学与临床, 2019, 39(6): 840-845.
[8]	宁娜侯晓鸿李杨何金玲燕子王晓晖王丽. 自噬降低激活β1-AA诱导的心肌细胞内质网应激相关凋亡途径[J]. 基础医学与临床, 2019, 39(1): 1-6.
[9]	严玉兰邵小美刘沙杭敏尹超云张日婷步雪峰. 重组新城疫病毒rL-IL29促进人小细胞肺癌细胞系H446内质网应激、自噬及凋亡相关蛋白的表达[J]. 基础医学与临床, 2018, 38(10): 1397-1402.
[10]	李丹婷刘露路高茹菲彭川杨淑敏胡金波肖晓秋李启富. 内质网应激参与双酚A导致小鼠的肝脏脂质沉积[J]. 基础医学与临床, 2016, 36(7): 886-890.
[11]	吴海江邓新娜史永红杜春阳韦金英任蕴卓段惠军. EGFR在高糖诱导下人肾小管上皮细胞凋亡中的作用[J]. 基础医学与临床, 2016, 36(2): 151-155.
[12]	雷艳任冰霜詹世淮孔旭辉黄梁浒. 沉默CHOP基因降低衣霉素诱导小鼠肝癌Hepa 1-6细胞凋亡[J]. 基础医学与临床, 2016, 36(12): 1646-1651.
[13]	胡深张洪义. 葡萄糖调节蛋白78在肝脏不同应激损伤时的作用[J]. 基础医学与临床, 2014, 34(12): 1710-1713.
[14]	董召刚张岩曲迅. 低氧微环境下内质网应激及其相关疾病[J]. 基础医学与临床, 2009, 29(6): 649-653.
[15]	杨燕丽向若兰孙琦. 内质网应激参与糖脂毒性引起的胰岛β细胞凋亡[J]. 基础医学与临床, 2009, 29(12): 1337-1340.