Login Register Cart 0
Research Article

巴特病尿胎贫血致胎儿心细胞损伤

卷 21, 期 2, 2021

发表于: 10 June, 2020

页: [165 - 175] 页: 11

弟呕挨: 10.2174/1566524020666200610163546

价格: $65

摘要

背景：严重的胎儿贫血会导致高输出心力衰竭。线粒体是心脏功能的关键调节器。但是，胎儿贫血的早期对胎儿心脏和心脏线粒体功能的影响尚不清楚。 目的：本研究的目的是比较贫血胎儿和非贫血胎儿的线粒体功能和胎儿心脏组织中的心脏生化变化。 材料与方法：在17-20周时对受Hb Bart病（n = 18）和非贫血胎儿（n = 10）影响的胎儿进行了横断面研究。在所有病例中均进行了超声心动图检查，以评估产前心脏功能。妊娠终止后收集心脏组织，以确定心脏铁的积累，线粒体功能，包括线粒体ROS的产生，线粒体去极化和线粒体肿胀，线粒体动力学，炎症和凋亡。 结果：Hb Bart和非贫血组通过超声评估的产前心脏功能相当。与非贫血组相比，巴特组的心脏线粒体去极化和肿胀水平以及TNF-α水平明显更高。相反，Hb Bart研究组的抗炎（IL-10）水平明显降低。此外，在Bart组中，活性caspase-3和Bcl-2的表达也显着较高（P = 0.001，P = 0.035）。 Bart组的线粒体裂变蛋白表达（包括p-DRP1 /总DRP1）明显更高。但是，两组之间的心脏铁蓄积水平没有差异。 结论：尽管Bart和非贫血组的产前心脏功能相当，心脏铁的蓄积量相当，但胎儿贫血与心脏线粒体功能障碍，线粒体裂变增加以及炎症和细胞凋亡增加显着相关。这些发现表明，在没有心脏铁超负荷的胎儿贫血的早期阶段，可导致患有Hb Bart的胎儿的心脏线粒体功能障碍。

关键词: 贫血，细胞凋亡，心脏组织，心脏功能，胎儿，血红蛋白，巴特氏病，线粒体功能，氧化应激。

« Previous Next »
[1]
Meriki N, Welsh AW. Technical considerations for measurement of the fetal left modified myocardial performance index. Fetal Diagn Ther 2012; 31(1): 76-80.
[http://dx.doi.org/10.1159/000334385] [PMID: 22236694]
[2]
Sikkel E, Klumper FJ, Oepkes D, et al. Fetal cardiac contractility before and after intrauterine transfusion. Ultrasound Obstet Gynecol 2005; 26(6): 611-7.
[http://dx.doi.org/10.1002/uog.1996] [PMID: 16254879]
[3]
Kumfu S, Chattipakorn SC, Fucharoen S, Chattipakorn N. Dual T-type and L-type calcium channel blocker exerts beneficial effects in attenuating cardiovascular dysfunction in iron-overloaded thalassaemic mice. Exp Physiol 2016; 101(4): 521-39.
[http://dx.doi.org/10.1113/EP085517] [PMID: 26824522]
[4]
Kumfu S, Chattipakorn S, Fucharoen S, Chattipakorn N. Mitochondrial calcium uniporter blocker prevents cardiac mitochondrial dysfunction induced by iron overload in thalassemic mice Biometals: an international journal on the role of metal ions in biology, biochemistry, and medicine 2012; 25(6): 1167-75.
[http://dx.doi.org/10.1007/s10534-012-9579-x]
[5]
Thummasorn S, Kumfu S, Chattipakorn S, Chattipakorn N. Granulocyte-colony stimulating factor attenuates mitochondrial dysfunction induced by oxidative stress in cardiac mitochondria. Mitochondrion 2011; 11(3): 457-66.
[http://dx.doi.org/10.1016/j.mito.2011.01.008] [PMID: 21292035]
[6]
Tsushima RG, Wickenden AD, Bouchard RA, Oudit GY, Liu PP, Backx PH. Modulation of iron uptake in heart by L-type Ca2+ channel modifiers: possible implications in iron overload. Circ Res 1999; 84(11): 1302-9.
[http://dx.doi.org/10.1161/01.RES.84.11.1302] [PMID: 10364568]
[7]
Kumfu S, Chattipakorn S, Fucharoen S, Chattipakorn N. Ferric iron uptake into cardiomyocytes of β-thalassemic mice is not through calcium channels. Drug Chem Toxicol 2013; 36(3): 329-34.
[http://dx.doi.org/10.3109/01480545.2012.726625] [PMID: 23050671]
[8]
Chua AC, Graham RM, Trinder D, Olynyk JK. The regulation of cellular iron metabolism. Crit Rev Clin Lab Sci 2007; 44(5-6): 413-59.
[http://dx.doi.org/10.1080/10408360701428257] [PMID: 17943492]
[9]
Oudit GY, Sun H, Trivieri MG, et al. L-type Ca2+ channels provide a major pathway for iron entry into cardiomyocytes in iron-overload cardiomyopathy. Nat Med 2003; 9(9): 1187-94.
[http://dx.doi.org/10.1038/nm920] [PMID: 12937413]
[10]
Wallander ML, Leibold EA, Eisenstein RS. Molecular control of vertebrate iron homeostasis by iron regulatory proteins. Biochim Biophys Acta 2006; 1763(7): 668-89.
[http://dx.doi.org/10.1016/j.bbamcr.2006.05.004] [PMID: 16872694]
[11]
Silva FH, Veiga FJR, Mora AG, et al. A novel experimental model of erectile dysfunction in rats with heart failure using volume overload. PLoS One 2017; 12(11)e0187083
[http://dx.doi.org/10.1371/journal.pone.0187083] [PMID: 29095897]
[12]
Pervaiz S. Redox pioneer: professor Barry Halliwell. Antioxid Redox Signal 2011; 14(9): 1761-6.
[http://dx.doi.org/10.1089/ars.2010.3518] [PMID: 20969479]
[13]
Matsushima S, Kinugawa S, Ide T, et al. Overexpression of glutathione peroxidase attenuates myocardial remodeling and preserves diastolic function in diabetic heart. Am J Physiol Heart Circ Physiol 2006; 291(5): H2237-45.
[http://dx.doi.org/10.1152/ajpheart.00427.2006] [PMID: 16844917]
[14]
Shiomi T, Tsutsui H, Matsusaka H, et al. Overexpression of glutathione peroxidase prevents left ventricular remodeling and failure after myocardial infarction in mice. Circulation 2004; 109(4): 544-9.
[http://dx.doi.org/10.1161/01.CIR.0000109701.77059.E9] [PMID: 14744974]
[15]
Zhou B, Tian R. Mitochondrial dysfunction in pathophysiology of heart failure. J Clin Invest 2018; 128(9): 3716-26.
[http://dx.doi.org/10.1172/JCI120849] [PMID: 30124471]
[16]
Kiyuna LA, Albuquerque RPE, Chen CH, Mochly-Rosen D, Ferreira JCB. Targeting mitochondrial dysfunction and oxidative stress in heart failure: Challenges and opportunities. Free Radic Biol Med 2018; 129: 155-68.
[http://dx.doi.org/10.1016/j.freeradbiomed.2018.09.019] [PMID: 30227272]
[17]
Dietl A, Maack C. Targeting Mitochondrial Calcium Handling and Reactive Oxygen Species in Heart Failure. Curr Heart Fail Rep 2017; 14(4): 338-49.
[http://dx.doi.org/10.1007/s11897-017-0347-7] [PMID: 28656516]
[18]
Münzel T, Camici GG, Maack C, Bonetti NR, Fuster V, Kovacic JC. Impact of Oxidative Stress on the Heart and Vasculature: Part 2 of a 3-Part Series. J Am Coll Cardiol 2017; 70(2): 212-29.
[http://dx.doi.org/10.1016/j.jacc.2017.05.035] [PMID: 28683969]
[19]
Niemann B, Rohrbach S, Miller MR, Newby DE, Fuster V, Kovacic JC. Oxidative Stress and Cardiovascular Risk: Obesity, Diabetes, Smoking, and Pollution: Part 3 of a 3-Part Series. J Am Coll Cardiol 2017; 70(2): 230-51.
[http://dx.doi.org/10.1016/j.jacc.2017.05.043] [PMID: 28683970]
[20]
Lian WS, Lin H, Cheng WT, Kikuchi T, Cheng CF. Granulocyte-CSF induced inflammation-associated cardiac thrombosis in iron loading mouse heart and can be attenuated by statin therapy. J Biomed Sci 2011; 18: 26.
[http://dx.doi.org/10.1186/1423-0127-18-26] [PMID: 21496220]
[21]
Mariappan N, Elks CM, Fink B, Francis J. TNF-induced mitochondrial damage: a link between mitochondrial complex I activity and left ventricular dysfunction. Free Radic Biol Med 2009; 46(4): 462-70.
[http://dx.doi.org/10.1016/j.freeradbiomed.2008.10.049] [PMID: 19041937]
[22]
Liesa M, Palacín M, Zorzano A. Mitochondrial dynamics in mammalian health and disease. Physiol Rev 2009; 89(3): 799-845.
[http://dx.doi.org/10.1152/physrev.00030.2008] [PMID: 19584314]
[23]
Chen H, Chan DC. Physiological functions of mitochondrial fusion. Ann N Y Acad Sci 2010; 1201: 21-5.
[http://dx.doi.org/10.1111/j.1749-6632.2010.05615.x] [PMID: 20649534]
[24]
Detmer SA, Chan DC. Functions and dysfunctions of mitochondrial dynamics. Nat Rev Mol Cell Biol 2007; 8(11): 870-9.
[http://dx.doi.org/10.1038/nrm2275] [PMID: 17928812]
[25]
Palaniyandi SS, Qi X, Yogalingam G, Ferreira JC, Mochly-Rosen D. Regulation of mitochondrial processes: a target for heart failure. Drug Discov Today Dis Mech 2010; 7(2): e95-e102.
[http://dx.doi.org/10.1016/j.ddmec.2010.07.002] [PMID: 21278905]
[26]
Pennanen C, Parra V, López-Crisosto C, et al. Mitochondrial fission is required for cardiomyocyte hypertrophy mediated by a Ca2+-calcineurin signaling pathway. J Cell Sci 2014; 127(Pt 12): 2659-71.
[http://dx.doi.org/10.1242/jcs.139394] [PMID: 24777478]

Rights & Permissions Print Cite
Article Metrics
22
1
© 2024 Bentham Science Publishers | Privacy Policy