[1]瞿珊珊?黄蓉蓉 闫军宇 李玉兰.线粒体功能障碍与平滑肌细胞表型转化的研究[J].心血管病学进展,2023,(4):360.[doi:10.16806/j.cnki.issn.1004-3934.2023.04.016]
 QU ShanshanHUANG RongrongYAN JunyuLI Yulan.Mitochondrial Functional Proteins Regulate Smooth Muscle Cell Phenotypic Transition and Cardiovascular Diseases[J].Advances in Cardiovascular Diseases,2023,(4):360.[doi:10.16806/j.cnki.issn.1004-3934.2023.04.016]
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线粒体功能障碍与平滑肌细胞表型转化的研究()
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《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2023年4期
页码:
360
栏目:
综述
出版日期:
2023-04-25

文章信息/Info

Title:
Mitochondrial Functional Proteins Regulate Smooth Muscle Cell Phenotypic Transition and Cardiovascular Diseases
作者:
瞿珊珊12?黄蓉蓉2 闫军宇1 李玉兰23
(1.兰州大学第一医院生殖医学中心,甘肃 兰州 730000;2.大学第一临床医学院,甘肃 兰州 7300003.兰州大学第一医院麻醉科,甘肃 兰州 730000)
Author(s):
QU Shanshan12HUANG RongrongYAN Junyu1LI Yulan23
(1.The Reproductive?Medicine CenterThe First Hospital of Lanzhou UniversityLanzhou 730000China2.The First School of Clinical MedicLanzhou UniversityLanzhou 730000China3.Department of AnesthesiologyThe First Hospital of Lanzhou UniversityLanzhou 730000China)
关键词:
平滑肌细胞表型转化线粒体功能钙稳态心血管疾病
Keywords:
Smooth muscle cellPhenotype transformationMitochondrial functionCalcium homeostasisCardiovascular diseases
DOI:
10.16806/j.cnki.issn.1004-3934.2023.04.016
摘要:
血管平滑肌细胞(VSMCs)具有两种表型——收缩型和合成型。VSMCs表型转化是心血管疾病早期病理改变的核心环节。近年研究发现线粒体功能是调节VSMCs表型的重要因素,其动力学及能量学的稳定直接影响VSMCs表型的转化,钙离子作为线粒体功能调节的重要因子参与其中。现综述线粒体功能改变调节VSMCs表型转化对心血管疾病的影响。
Abstract:
There are two phenotypes of vascular smooth muscle cells (VSMCs): contractile and synthetic. VSMCs phenotypic transformation is a central aspect of early pathological changes in cardiovascular diseases. Recent studies have identified mitochondrial function as an important factor in regulating VSMCs phenotype. VSMCs phenotypic conversion is directly influenced by its dynamics and energy stability,in which calcium ions are involved as an important factor in the regulation of mitochondrial function. This paper reviews the impact of mitochondrial functional changes on the regulation of VSMCs phenotypic transition in cardiovascular disease.

参考文献/References:

[1] Takaichi S,Yutani C,Fujita H,et al. Ultrastructural studies on the phenotypic modulation of human intimal smooth muscle cells[J]. Atherosclerosis,1993,100(2):197-211.[2] Jin L,Lin X,Yang L,et al. AK098656,a novel vascular smooth muscle cell-dominant long noncoding RNA,promotes hypertension[J]. Hypertension,2018,71(2):262-272. [3] Zhu Q,Ni XQ,Lu WW,et al. Intermedin reduces neointima formation by regulating vascular smooth muscle cell phenotype via cAMP/PKA pathway[J]. Atherosclerosis,2017,266:212-222.[4] Allahverdian S,Chaabane C,Boukais K,et al. Smooth muscle cell fate and plasticity in atherosclerosis[J]. Cardiovasc Res,2018,114(4):540-550.[5] Quiles-Jiménez A,Gregersen I,Segers FM,et al. DNA glycosylase Neil3 regulates vascular smooth muscle cell biology during atherosclerosis development[J]. Atherosclerosis,2021,324:123-132. [6] Touyz RM,Alves-Lopes R,Rios FJ,et al. Vascular smooth muscle contraction in hypertension[J]. Cardiovasc Res,2018,114(4):529-539. [7] 廖静雯,张琳,张严焱,等. 高血压和增龄对大鼠小动脉平滑肌表型转换和miR-143/145表达的影响[J]. 中国动脉硬化杂志,2017,25(3):230-237.[8] Mulvany MJ. Small artery remodelling in hypertension[J]. Basic Clin Pharmacol Toxicol,2012,110(1):49-55.[9] Yapa NMB,Lisnyak V,Reljic B,et al. Mitochondrial dynamics in health and disease[J]. FEBS Lett,2021,595(8):1184-1204.[10] Salabei JK,Hill BG. Mitochondrial fission induced by platelet-derived growth factor regulates vascular smooth muscle cell bioenergetics and cell proliferation[J]. Redox Biol,2013,1(1):542-551.[11] Emery JM,Ortiz RM. Mitofusin 2:a link between mitochondrial function and substrate metabolism?[J]. Mitochondrion,2021,61:125-137.[12] 文禹粱,刘秀,王继卿,等. 哺乳动物线粒体动力学和氧化磷酸化研究进展[J]. 畜牧兽医学报,2021,52(2):273-285. [13] Fang X,Chen X,Zhong GW,et al. Mitofusin 2 downregulation triggers pulmonary artery smooth muscle cell proliferation and apoptosis imbalance in rats with hypoxic pulmonary hypertension via the PI3K/Akt and mitochondrial apoptosis pathways[J]. J Cardiovasc Pharmacol,2016,67(2):164-174.[14] Gu Y,Yu X,Li X,et al. Inhibitory effect of mabuterol on proliferation of rat ASMCs induced by PDGF-BB via regulating [Ca2+]i and mitochondrial fission/fusion[J]. Chem Biol Interact,2019,307:63-72.[15] Torres G,Morales PE,García-Miguel M,et al. Glucagon-like peptide-1 inhibits vascular smooth muscle cell dedifferentiation through mitochondrial dynamics regulation[J]. Biochem Pharmacol,2016,104:52-61. [16] 牛艳华. 脂肪酸合酶抑制剂改善肺动脉高压线粒体损伤的作用机制研究[D]. 上海:上海交通大学,2019. [17] Wang F,Zhen Y,Si C,et al. WNT5B promotes vascular smooth muscle cell dedifferentiation via mitochondrial dynamics regulation in chronic thromboembolic pulmonary hypertension[J]. J Cell Physiol,2022,237(1):789-803.[18] Marsboom G,Toth PT,Ryan JJ,et al. Dynamin-related protein 1-mediated mitochondrial mitotic fission permits hyperproliferation of vascular smooth muscle cells and offers a novel therapeutic target in pulmonary hypertension[J]. Circ Res,110(11):1484-1497.[19] Zhang X,Chen W,Li J,et al. Involvement of mitochondrial fission in calcium sensing receptor-mediated vascular smooth muscle cells proliferation during hypertension[J]. Biochem Biophys Res Commun,2018,495(1):454-460. [20] Deng Y,Li S,Chen Z,et al. Mdivi-1,a mitochondrial fission inhibitor,reduces angiotensin-II- induced hypertension by mediating VSMC phenotypic switch[J]. Biomed Pharmacother,2021,140:111689.[21] Li H,Horke S,F?stermann U. Vascular oxidative stress,nitric oxide and atherosclerosis[J]. Atherosclerosis,2014,237(1):208-219. [22] Scheede-Bergdahl C,Bergdahl A. Adaptation of mitochondrial expression and ATP production in dedifferentiating vascular smooth muscle cells[J]. Can J Physiol Pharmacol,2017,95(12):1473-1479.[23] Yu EPK,Reinhold J,Yu H,et al. Mitochondrial respiration is reduced in atherosclerosis,promoting necrotic core formation and reducing relative fibrous cap thickness[J]. Arterioscler Thromb Vasc Biol,2017,37(12):2322-2332.[24] Chu J,Tong M,de la Monte SM. Chronic ethanol exposure causes mitochondrial dysfunction and oxidative stress in immature central nervous system neurons[J]. Actor Neuropathologica,2007,113(6):659-673.[25] 刘井波,彭双清,阳海鹰,等. 丁烯酸内酯对心肌线粒体呼吸链酶复合物活力的影响[J]. 卫生毒理学杂志,2005,19(1):18-20.[26] Jia Y,Wang M,Mao C,et al. COMP-prohibitin 2 interaction maintains mitochondrial homeostasis and controls smooth muscle cell identity[J]. Cell Death Dis,2018,9(6):676.[27] Strub GM,Paillard M,Liang J,et al. Sphingosine-1-phosphate produced by sphingosine kinase 2 in mitochondria interacts with prohibitin 2 to regulate complex IV assembly and respiration[J]. FASEB J,2011,25(2):600-612. [28] Yao CH,Wang R,Wang Y,et al. Mitochondrial fusion supports increased oxidative phosphorylation during cell proliferation[J]. Elife,2019,8:e41351. [29] Hong Z,Chen KH,DasGupta A,et al. microRNA-138 and microRNA-25 down-regulate mitochondrial calcium uniporter,causing the pulmonary arterial hypertension cancer phenotype[J]. Am J Respir Crit Care Med,2017,195(4):515-529. [30] 徐欢成,郑明学,古少鹏,等. 钙信号转导对细胞凋亡的影响[J]. 动物医学进展,2013,34(1):112-115.[31] Bravo R,Vicencio JM,Parra V,et al. Increased ER-mitochondrial coupling promotes mitochondrial respiration and bioenergetics during early phases of ER stress[J]. J Cell Sci,2011,124(Pt 13):2143-2152.[32] Paupe V,Prudent J. New insights into the role of mitochondrial calcium homeostasis in cell migration[J]. Biochem Biophys Res Commun,2018,500(1):75-86. [33] Giorgi C,Marchi S,Pinton P. Publisher correction:the machineries,regulation and cellular functions of mitochondrial calcium[J]. Nat Rev Mol Cell Biol,2018,19(11):746. [34] Rossi A,Pizzo P,Filadi R. Calcium,mitochondria and cell metabolism:a functional triangle in bioenergetics[J]. Biochim Biophys Acta Mol Cell Res,2019,1866(7):1068-1078. [35] Kowaltowski AJ,Menezes-Filho SL,Assali EA,et al. Mitochondrial morphology regulates organellar Ca2+?ptake and changes cellular Ca2+?omeostasis[J]. FASEB J,2019,33(12):13176-13188.[36] Chen Y,Csordás G,Jowdy C,et al. Mitofusin 2-containing mitochondrial-reticular microdomains direct rapid cardiomyocyte bioenergetic responses via interorganelle Ca(2+) crosstalk[J]. Circ Res,2012,111(7):863-875. [37] Strubbe-Rivera JO,Schrad JR,Pavlov EV,et al. The mitochondrial permeability transition phenomenon elucidated by cryo-EM reveals the genuine impact of calcium overload on mitochondrial structure and function[J]. Sci Rep,2021,11(1):1037.[38] Phadwal K,Vrahnas C,Ganley IG,et al. Mitochondrial dysfunction:cause or consequence of vascular calcification?[J]. Front Cell Dev Biol,2021,9:611922. [39] Marchi S,Patergnani S,Missiroli S,et al. Mitochondrial and endoplasmic reticulum calcium homeostasis and cell death[J]. Cell Calcium,2018,69:62-72.

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备注/Memo

备注/Memo:
收稿日期:2022-10-26基金项目:lzuyxcx-2022-186)
更新日期/Last Update: 2023-05-17