2025年5月25日 周日
Home > Archive>Volume 30, Issue 6, 2022 >470-475
PDF HTML XML Export Cite reminder
Mitochondria and its protein quality control disorder and atherosclerosis
Author:
Affiliation:

1.Key Laboratory of Traditional Chinese Medicine Visceral Image Theory and Application, Ministry of Education, Liaoning University of Traditional Chinese Medicine, Shenyang, Liaoning 110847, China;2.Traditional Chinese Medicine College, Liaoning University of Traditional Chinese Medicine, Shenyang, Liaoning 110847, China;3.Laboratory of Mitochondrial Biology and Medicine, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China)

Clc Number:

R5

  • Article
    • | |
  • Metrics
    • |
  • Reference [51]
    • | | | |
  • Comments
    Abstract:

    Mitochondria are important organelles in mammalian cells. As the regulatory center of cell energy metabolism and cell death, mitochondrial dysfunction will lead to the occurrence and development of a variety of diseases. Mitochondrial function depends on the integrity and homeostasis of mitochondrial proteome. Therefore, mitochondrial protein quality control system is very important to maintain mitochondrial homeostasis and body health. When mitochondria and their protein quality control system are abnormal, it will directly damage mitochondria and lead to abnormal mitochondrial protein accumulation, resulting in intracellular environmental disorder and even cell dysfunction, which may affect the occurrence and development of atherosclerotic diseases. This paper reviews the role of mitochondria and its protein quality control system in the occurrence and development of atherosclerotic diseases, and looks forward to the future development prospects and challenges in this field, in order to providing scientific evidence for finding specific mitochondrial protein closely related to atherosclerotic diseases.

    Reference
    [1] BENJAMIN E J, BLAHA M J, CHIUVE S E, et al.Heart disease and stroke statistics-2017 update a report from the American Heart Association.Circulation, 7,5(10):E146-E603.
    [2] GAO S, ZHAO D, WANG M, et al.Association between circulating oxidized LDL and atherosclerotic cardiovascular disease:a Meta-analysis of observational studies.Can J Cardiol, 7,3(12):1624-1632.
    [3] 彭文夕, 蔡国鼎, 陈金娜, 等.能量代谢异常与动脉粥样硬化.生命的化学, 9,9(2):273-278.
    [4] WALLACE D C.Mitochondria and cancer.Nat Rev Cancer, 2,2(10):685-698.
    [5] RUGARLI E I, LANGER T.Mitochondrial quality control:a matter of life and death for neurons.EMBO J, 2,1(6):1336-1349.
    [6] 高磊, 张欣, 刘越.血管内皮细胞线粒体动力学相关功能与心血管疾病关系的研究进展.心脏杂志, 7,9(1):105-108.
    [7] 吴繁, 刘莉, 金娟, 等.线粒体质量控制与心血管疾病.国际心血管病杂志, 1,8(3):160-162.
    [8] 张泽.线粒体动力学与肿瘤的研究进展.复旦学报(医学版), 9,6(1):128-134.
    [9] 黄健, 姜小凡, 叶莉斯.线粒体动力学研究进展.吉林医药学院学报, 8,9(5):371-373.
    [10] ZHENG J, LU C.Oxidized LDL causes endothelial apoptosis by inhibiting mitochondrial fusion and mitochondria autophagy.Front Cell Dev Biol, 0,8:600950.
    [11] FORTE M, SCHIRONE L, AMERI P, et al.The role of mitochondrial dynamics in cardiovascular diseases.Br J Pharmacol, 1,8(10):2060-2076.
    [12] WANG Y, SUBRAMANIAN M, YURDAGUL A J, et al.Mitochondrial fission promotes the continued clearance of apoptotic cells by macrophages.Cell, 7,1(2):331-345.e22.
    [13] WANG Q L, ZHANG M, TORRES G, et al.Metformin suppresses diabetes-accelerated atherosclerosis via the inhibition of Drp1-mediated mitochondrial fission.Diabetes, 7,6(1):193-205.
    [14] ROGERS M A, MALDONADO N, HUTCHESON J D, et al.Dynamin-related protein 1 inhibition attenuates cardiovascular calcification in the presence of oxidative stress.Circ Res, 7,1(3):220-233.
    [15] LIM S, LEE S Y, SEO H H, et al.Regulation of mitochondrial morphology by positive feedback interaction between PKCδ and Drp1 in vascular smooth muscle cell.J Cell Biochem, 5,6(4):648-660.
    [16] YANG J, ZHOU X, ZENG X, et al.Resveratrol attenuates oxidative injury in human umbilical vein endothelial cells through regulating mitochondrial fusion via TyrRS-PARP1 pathway.Nutr Metab (Lond), 9,6:9.
    [17] LEMASTERS J J.Selective mitochondrial autophagy, or mitophagy,as a targeted defense against oxidative stress,mitochondrial dysfunction, and aging.Rejuvenation Res, 5,8(1):3-5.
    [18] VIVES-BAUZA C, ZHOU C, HUANG Y, et al.PINK1-dependent recruitment of Parkin to mitochondria in mitophagy.Proc Nat Acad Sci USA, 0,7(1):378-383.
    [19] 程婧, 魏林, 李苗.线粒体动力学及线粒体自噬调控机制的研究进展.生理学报, 0,2(4):475-487.
    [20] 张妍, 刘昉.线粒体动力学和线粒体自噬与心血管疾病的研究进展.中国心血管病研究, 1,9(2):169-174.
    [21] 刘晓鹏.新型经导管置入主动脉瓣膜临床前研究及线粒体自噬对动脉粥样硬化保护机制研究.北京:北京协和医学院, 2016.
    [22] PENG X, CHEN H, LI Y, et al.Effects of NIX-mediated mitophagy on ox-LDL-induced macrophage pyroptosis in atherosclerosis.Cell Biol Int, 0,4(7):1481-1490.
    [23] ZHENG J, LU C.Oxidized LDL causes endothelial apoptosis by inhibiting mitochondrial fusion and mitochondria autophagy.Front Cell Dev Biol, 0,8:600950.
    [24] LI P, WANG J, ZHAO X, et al.PTEN inhibition attenuates endothelial cell apoptosis in coronary heart disease via modulating the AMPK-CREB-Mfn2-mitophagy signaling pathway.J Cell Physiol, 0,5(5):4878-4889.
    [25] HE L, ZHOU Q, HUANG Z, et al.PINK1/parkin-mediated mitophagy promotes apelin-13-induced vascular smooth muscle cell proliferation by AMPKα and exacerbates atherosclerotic lesions.J Cell Physiol, 9,4(6):8668-8682.
    [26] DOCHERTY C K, CARSWELL A, FRIEL E, et al.Impaired mitochondrial respiration in human carotid plaque atherosclerosis:a potential role for PINK1 in vascular smooth muscle cell energetics.Atherosclerosis, 8,8:1-11.
    [27] TYRRELL D J, BLIN M G, SONG J, et al.Age-associated mitochondrial dysfunction accelerates atherogenesis.Circ Res, 0,6(3):298-314.
    [28] KATTOOR A J, POTHINENI N V, PALAGIRI D, et al.Oxidative stress in atherosclerosis.Curr Atheroscler Rep, 7,9(11):42.
    [29] MA S, CHEN J, FENG J, et al.Melatonin ameliorates the progression of atherosclerosis via mitophagy activation and NLRP3 inflammasome inhibition.Oxid Med Cell Longev, 2018:9286458.
    [30] BOLAND M L, CHOURASIA A H, MACLEOD K F.Mitochondrial dysfunction in cancer.Front Oncol, 3,3:292.
    [31] ZHU J, WANG K Z, CHU C T.After the banquet:mitochondrial biogenesis, mitophagy, and cell survival.Autophagy, 3,9(11):1663-1676.
    [32] 袁清, 刘江华, 曾召林.线粒体功能障碍在代谢性炎症中的作用.江苏大学学报(医学版), 1,1(5):448-454.
    [33] XUE Y, WEI Z, DING H, et al.MicroRNA-19b/221/222 induces endothelial cell dysfunction via suppression of PGC-1α in the progression of atherosclerosis.Atherosclerosis, 5,1(2):671-681.
    [34] SHIMBA Y, TOGAWA H, SENOO N, et al.Skeletal muscle-specific PGC-1α overexpression suppresses atherosclerosis in apolipoprotein E-knockout mice.Sci Rep, 9,9(1):4077.
    [35] WANG G, YANG Y, MA H, et al.LncRNA FENDRR inhibits ox-LDL induced mitochondrial energy metabolism disorder in aortic endothelial cells via miR-18a-5p/PGC-1α signaling pathway.Front Endocrinol (Lausanne), 1,2:622665.
    [36] PENG W, CAI G, XIA Y, et al.Mitochondrial dysfunction in atherosclerosis.DNA Cell Biol, 9,8(7):597-606.
    [37] TSAI K L, HUNG C H, CHAN S H, et al.Chlorogenic acid protects against oxLDL-induced oxidative damage and mitochondrial dysfunction by modulating SIRT1 in endothelial cells.Mol Nutr Food Res, 8,2(11):e1700928.
    [38] CHEN S, DING Y, ZHANG Z, et al.Hyperlipidaemia impairs the circadian clock and physiological homeostasis of vascular smooth muscle cells via the suppression of Smarcd1.J Pathol, 4,3(2):159-169.
    [39] KARNEWAR S, VASAMSETTI S B, GOPOJU R, et al.Mitochondria-targeted esculetin alleviates mitochondrial dysfunction by AMPK-mediated nitric oxide and SIRT3 regulation in endothelial cells:potential implications in atherosclerosis.Sci Rep, 6,6:24108.
    [40] PEREZ-TERNERO C, WERNER C M, NICKEL A G, et al.Ferulic acid, a bioactive component of rice bran, improves oxidative stress and mitochondrial biogenesis and dynamics in mice and in human mononuclear cells.J Nutr Biochem, 7,8:51-61.
    [41] 庄天鹏, 魏曼丽, 贾振伟.线粒体蛋白质组及蛋白质量控制.中国细胞生物学学报, 1,3(1):161-169.
    [42] HERRINGTON D M, MAO C, PARKER S J, et al.Proteomic architecture of human coronary and aortic atherosclerosis.Circulation, 8,7(25):2741-2756.
    [43] LEBEAU J, RAINBOLT T K, WISEMAN R L.Coordinating mitochondrial biology through the stress-responsive regulation of mitochondrial proteases.Int Rev Cell Mol Biol, 8,0:79-128.
    [44] 程思源, 张苑, 陈磊磊.泛素-蛋白酶体系统在心血管疾病中的研究进展.医学综述, 8,4(15):2954-2960.
    [45] LIAO J, YANG X, LIN Q, et al.Inhibition of the ubiquitin-activating enzyme UBA1 suppresses diet-induced atherosclerosis in apolipoprotein E-knockout mice.J Immunol Res, 2020.DOI:10.1155/2020/7812709.
    [46] DONG M, ZHANG Y, XU C, et al.Interferon-γ decreases ATP-binding cassette subfamily G member 1-mediated cholesterol efflux through small ubiquitin-like modifier/ubiquitin-dependent liver X receptor-α degradation in macrophages.Biotechnol Appl Biochem, 1,8(6):1412-1420.
    [47] KIM S, LEE W, CHO K.P62 links the autophagy pathway and the ubiquitin-proteasome system in endothelial cells during atherosclerosis.Int J Mol Sci, 1,2(15):7791.
    [48] QUIRS P M, LANGER T, LPEZ-OTN C.New roles for mitochondrial proteases in health, ageing and disease.Nat Rev Mol Cell Biol, 5,6(6):345-359.
    [49] ONAT U, YILDIRIM A D, TUFANLI , et al.Intercepting the lipid-induced integrated stress response reduces atherosclerosis.J Am Coll Cardiol, 9,3(10):1149-1169.
    [50] BHASKARAN S, PHARAOH G, RANJIT R, et al.Loss of mitochondrial protease ClpP protects mice from diet-induced obesity and insulin resistance.EMBO Rep, 8,9(3):e45009.
    [51] SONG Y, XU Y, LIU Y, et al.Mitochondrial quality control in the maintenance of cardiovascular homeostasis:the roles and interregulation of UPS, mitochondrial dynamics and mitophagy.Oxid Med Cell Longev, 2021.DOI:10.1155/2021/3960773.
    Related
    Cited by
    Comments
    Comments
    分享到微博
    Submit
Get Citation

WU Jin, CHEN Lijuan, YUAN Dongchao, WANG Yu, DU Ying, WANG Shuang, ZHANG Zhe, JIA Lianqun, LYU Bin, YANG Guanlin. Mitochondria and its protein quality control disorder and atherosclerosis[J]. Editorial Office of Chinese Journal of Arteriosclerosis,2022,30(6):470-475.

Copy
Share
Article Metrics
  • Abstract:952
  • PDF: 848
  • HTML: 0
  • Cited by: 0
History
  • Received:July 08,2021
  • Revised:November 24,2021
  • Online: May 10,2022
Article QR Code

You are the 48713 visitor

Post Code：421001 Fax：0734-8160523

Phone：0734-8160765 E-mail：dmzzbjb@163.net

Editorial Office of Chinese Journal of Arteriosclerosis ® 2025