肺动脉高压与心肌电重塑的发生机制的研究进展

doi:10.20047/j.issn1673-7210.2023.31.08

摘要
图/表
参考文献
相关文章 (15)

全文: PDF (537 KB) HTML (1 KB)
输出: BibTeX | EndNote (RIS)

摘要肺动脉高压（PAH）系肺动脉压、肺血管阻力增高致使患者右心室衰竭（RVF）甚至死亡的一种疾病。RVF为PAH患者最常见死亡原因，大量研究表明，PAH患者RVF进程中涉及一系列心肌重塑，包括心脏结构重塑、机械重塑及心肌电重塑，而心肌电重塑为患者合并恶性心律失常及导致心源性猝死的重要原因。近年来有许多关于PAH的分子遗传学及细胞生物学研究，本文对其中所包含的上游病理生理学机制及心肌电重塑在PAH发病机制中的生物功能和作用作一综述，为PAH临床治疗提供新靶标。

	服务

	把本文推荐给朋友
	加入我的书架
	加入引用管理器
	E-mail Alert
	RSS
	作者相关文章
	覃思润　　陈晨阳　　曹宇

关键词 ：肺动脉高压, 心肌电重塑, 发生机制, 研究进展

Abstract：Pulmonary arterial hypertension (PAH) is a disease that increases pulmonary arterial pressure and pulmonary vascular resistance leading to right ventricular failure (RVF) or even death of patients. RVF is the most common cause of death in patients with PAH. A large number of studies have shown that the process of RVF in PAH patients involves a series of myocardial remodeling, including cardiac structural remodeling, mechanical remodeling, and myocardial electrical remodeling, and myocardial electrical remodeling is an important cause of patients with malignant arrhythmia and sudden cardiac death. In recent years, there have been many studies on the molecular genetics and cell biology of PAH. This article reviews the upstream pathophysiological mechanism and the biological function and role of myocardial electrical remodeling in the pathogenesis of PAH, so as to provide new targets for the clinical treatment of PAH.

Key words： Pulmonary artery hypertension Myocardial electrical remodeling Occurrence mechanism Research progress

基金资助:国家自然科学基金资助项目（82000300）。

通讯作者: 陈晨阳（1989.1-），男，博士；研究方向：肺动脉高压、动脉粥样硬化。曹宇（1975.8-），男，博士，副教授，主任医师；研究方向：冠心病、动脉粥样硬化、肺动脉高压。

引用本文:

覃思润　　陈晨阳　　曹宇. 肺动脉高压与心肌电重塑的发生机制的研究进展[J]. 中国医药导报, 2023, 20(31): 44-47.
QIN Sirun CHEN Chenyang CAO Yu. Research progress on the mechanism of pulmonary hypertension and myocardial electrical remodeling. 中国医药导报, 2023, 20(31): 44-47.

链接本文:

https://www.yiyaodaobao.com.cn/CN/10.20047/j.issn1673-7210.2023.31.08 或 https://www.yiyaodaobao.com.cn/CN/Y2023/V20/I31/44

[1] Ruopp NF，Cockrill BA. Diagnosis and Treatment of Pulmonary Arterial Hypertension：A Review [J]. JAMA，2022， 327（14）：1379-1391.
[2] Cirulis MM，Ryan JJ，Archer SL. Pathophysiology，incidence，management，and consequences of cardiac arrhythmia in pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension [J]. Pulm Circ，2019，9（1）： 204589 4019834890.
[3] Xue L，Yang YC，Zhao Q，et al. The spectrum and prevalence of arrhythmia in different clinical pulmonary hypertension groups in Chinese population [J]. Clin Cardiol，2022，45（5）：495-502.
[4] Vachiéry JL，Tedford RJ，Rosenkranz S，et al. Pulmonary hypertension due to left heart disease [J]. Eur Respir J，2019， 53（1）：1801897-1801908.
[5] Gewehr DM，Giovanini AF，Mattar BA，et al. Congestive Hepatopathy Secondary to Right Ventricular Hypertrophy Related to Monocrotaline-Induced Pulmonary Arterial Hypertension [J]. Int J Mol Sci，2021，22（21）：11891-11907.
[6] Jefri M，Bell S，Peng H，et al. Stimulation of L-type calcium channels increases tyrosine hydroxylase and dopamine in ventral midbrain cells induced from somatic cells [J]. Stem Cells Transl Med，2020，9（6）：697-712.
[7] Hassan MT，Lytton J. Potassium-dependent sodium-calcium exchanger（NCKX）isoforms and neuronal function [J]. Cell Calcium，2020，86：102-135.
[8] Hegyi B，P?觟l?觟nen RP，Hellgren KT，et al. Cardiomyocyte Na+ and Ca2+ mishandling drives vicious cycle involving CaMKⅡ，ROS，and ryanodine receptors [J]. Basic Res Cardiol，2021， 116（1）：58.
[9] Middleton JT，Maulik A，Lewis R，et al. Arrhythmic Burden and Outcomes in Pulmonary Arterial Hypertension [J]. Front Med（Lausanne），2019，23（6）：169-177.
[10] Witte C，Meyer Zur Heide Genannt Meyer-Arend JU，Andrié R，et al. Heart Rate Variability and Arrhythmic Burden in Pulmonary Hypertension [J]. Adv Exp Med Biol，2016，934： 9-22.
[11] Almorós AL，Cepeda-Rodrigo JM，Lorenzo ■，et al. Diabetic cardiomyopathy [J]. Rev Clin Esp（Barc），2022，222（2）：100-111.
[12] Wallace SR，Pagano PJ，Kra■un D，et al. MicroRNAs in the Regulation of NADPH Oxidases in Vascular Diabetic and Ischemic Pathologies：A Case for Alternate Inhibitory Strategies？[J] Antioxidants（Basel），2022，12（1）：70-84.
[13] Powers KG，Ma XM，Eipper BA，et al. Cell-type specific knockout of peptidylglycine α-amidating monooxygenase reveals specific behavioral roles in excitatory forebrain neurons and cardiomyocytes [J]. Genes Brain Behav，2021，20（2）：e12699.
[14] Wang K，Zhao J，Guo Z，et al. Interaction of KCNA5，CX43，and CX40 proteins in the atrial muscle of patients with atrial fibrillation [J]. Cell Biol Int，2022，46（11）：1834-1840.
[15] Tang C，Luo YM，Li S，et al. Characteristics of inflammation process in monocrotaline-induced pulmonary arterial hyper- tension in rats [J]. Biomed Pharmacother，2021，133（2021）：111081-111089.
[16] Dabral S，Muecke C，Valasarajan C，et al. A RASSF1A- HIF1α loop drives Warburg effect in cancer and pulmonary hypertension [J]. Nat Commun，2019，10（1）：21-30.
[17] Houten SM，Violante S，Ventura FV，et al. The biochemistry and physiology of mitochondrial fatty acid β-oxidation and its genetic disorders [J]. Annu Rev Physiol，2016， 78：23-44.
[18] Maguolo A，Rodella G，Dianin A，et al. Diagnosis，genetic characterization and clinical follow up of mitochondrial fatty acid oxidation disorders in the new era of expanded newborn screening：A single centre experience [J]. Mol Genet Metab Rep，2020，24（2020）：100632-100640.
[19] Zheng Y，Hu Q，Wu J，et al. Adiponectin ameliorates placental injury in gestational diabetes mice by correcting fatty acid oxidation/peroxide imbalance-induced ferroptosis via restoration of CPT-1 activity [J]. Endocrine，2022，75（3）：781-793.
[20] Hwang JS，Kim E，Lee HG，et al. Peroxisome proliferator-activated receptor δ rescues xCT-deficient cells from ferroptosis by targeting peroxisomes [J]. Biomed Pharmacother，2021，143：112-223.
[21] Fowler ED，Wang N，Hezzell MJ，et al. Improved Ca2+ release synchrony following selective modification of Itof and phase 1 repolarization in normal and failing ventricular myocytes [J]. J Mol Cell Cardiol，2022，172：52-62.
[22] Liu P，Bao HY，Jin CC，et al. Targeting extracellular heat shock protein 70 ameliorates doxorubicin-induced heart failure through resolution of toll-like receptor 2-mediated myocardial inflammation [J]. J Am Heart Assoc，2019，8（20）：e012338-e012348.
[23] Wu DC，Dasgupta A，Read AD，et al. Oxygen sensing，mitochondrial biology and experimental therapeutics for pulmonary hypertension and cancer [J]. Free Radic Biol Med，2021，170：150-178.
[24] Xu D，Hu YH，Gou X，et al. Oxidative Stress and Antioxidative Therapy in Pulmonary Arterial Hypertension [J]. Molecules，2022，27（12）：3724-3752.
[25] Saadeh K，Fazmin IT. Mitochondrial Dysfunction Increases Arrhythmic Triggers and Substrates; Potential Anti-arrhythmic Pharmacological Targets [J]. Front Cardiovasc Med，2021，15（8）：646-932.
[26] Conza GD，Ho PC. ER Stress Responses：An Emerging Modulator for Innate Immunity [J]. Cells，2020，9（3）：695-705.
[27] Liu M，Shi G，Zhou A，et al. Activation of the unfolded protein response downregulates cardiac ion channels in human induced pluripotent stem cell-derived cardiomyocytes [J]. J Mol Cell Cardiol，2018，117：62-71.
[28] Gao X，Gao S，Guan Y，et al. Toll-like receptor 3 controls QT interval on the electrocardiogram by targeting the degradation of Kv4. 2/4.3 channels in the endoplasmic reticulum [J]. FASEB J，2019，33（5）：6197-6208.
[29] Mandula JK，Chang S，Mohamed E，et al. Ablation of the endoplasmic reticulum stress kinase PERK induces paraptosis and type I interferon to promote anti-tumor T cell responses [J]. Cancer Cell，2022，40（10）：1145-1160.
[30] Fowler ED，Drinkhill MJ，Norman R，et al. Beta1-adrenoceptor antagonist，metoprolol attenuates cardiac myocyte Ca2+ handling dysfunction in rats with pulmonary artery hypertension [J]. J Mol Cell Cardiol，2018，120：74-83.
[31] Ma Y，Wang W，Devarakonda T，et al. Functional analysis of molecular and pharmacological modulators of mitochondrial fatty acid oxidation [J]. Sci Rep，2020，10（1）：1450.