본문 바로가기
KERD
논문KCI 등재

Unbalanced Redox With Autophagy in Cardiovascular Disease

2

조회

0

다운로드

0

인용

0

참고문헌

키워드

초록

Precise redox balance is essential for the optimum health and physiological function of the human body. Furthermore, an unbalanced redox state is widely believed to be part of numerous diseases, ultimately resulting in death. In this review, we discuss the relationship between redox balance and cardiovascular disease (CVD). In various animal models, excessive oxidative stress has been associated with increased atherosclerotic plaque formation, which is linked to the inflammation status of several cell types. However, various antioxidants can defend against reactive oxidative stress, which is associated with an increased risk of CVD and mortality. The different cardiovascular effects of these antioxidants are presumably due to alterations in the multiple pathways that have been mechanistically linked to accelerated atherosclerotic plaque formation, macrophage activation, and endothelial dysfunction in animal models of CVD, as well as in in vitro cell culture systems. Autophagy is a regulated cell survival mechanism that removes dysfunctional or damaged cellular organelles and recycles the nutrients for the generation of energy. Furthermore, in response to atherogenic stress, such as the generation of reactive oxygen species, oxidized lipids, and inflammatory signaling between cells, autophagy protects against plaque formation. In this review, we characterize the broad spectrum of oxidative stress that influences CVD, summarize the role of autophagy in the content of redox balance-associated pathways in atherosclerosis, and discuss potential therapeutic approaches to target CVD by stimulating autophagy.

Abstract

Precise redox balance is essential for the optimum health and physiological function of the human body. Furthermore, an unbalanced redox state is widely believed to be part of numerous diseases, ultimately resulting in death. In this review, we discuss the relationship between redox balance and cardiovascular disease (CVD). In various animal models, excessive oxidative stress has been associated with increased atherosclerotic plaque formation, which is linked to the inflammation status of several cell types. However, various antioxidants can defend against reactive oxidative stress, which is associated with an increased risk of CVD and mortality. The different cardiovascular effects of these antioxidants are presumably due to alterations in the multiple pathways that have been mechanistically linked to accelerated atherosclerotic plaque formation, macrophage activation, and endothelial dysfunction in animal models of CVD, as well as in in vitro cell culture systems. Autophagy is a regulated cell survival mechanism that removes dysfunctional or damaged cellular organelles and recycles the nutrients for the generation of energy. Furthermore, in response to atherogenic stress, such as the generation of reactive oxygen species, oxidized lipids, and inflammatory signaling between cells, autophagy protects against plaque formation. In this review, we characterize the broad spectrum of oxidative stress that influences CVD, summarize the role of autophagy in the content of redox balance-associated pathways in atherosclerosis, and discuss potential therapeutic approaches to target CVD by stimulating autophagy.

참고문헌 (169)

  1. Khosravi M, "The effects of oxidative stress on the development of atherosclerosis", Biol Chem, 400, pp.711~732 (2019)
  2. Hopkins BL, "Redoxins as gatekeepers of the transcriptional oxidative stress response", Redox Biol, 21, pp.101104~ (2019)
  3. Seifried HE, "A review of the interaction among dietary antioxidants and reactive oxygen species", J Nutr Biochem, 18, pp.567~579 (2007)
  4. Sies H, "Reactive oxygen species(ROS)as pleiotropic physiological signalling agents", Nat Rev Mol Cell Biol, 21, pp.363~383 (2020)
  5. Kamata H, "Redox regulation of cellular signalling", Cell Signal, 11, pp.1~14 (1999)
  6. Yang S, "ROS and diseases : role in metabolism and energy supply", Mol Cell Biochem, 467, pp.1~12 (2020)
  7. Birben E, "Oxidative stress and antioxidant defense", World Allergy Organ J, 5, pp.9~19 (2012)
  8. Rhee SG, "Hydrogen peroxide : a key messenger that modulates protein phosphorylation through cysteine oxidation", Sci STKE, 2000, pp.pe1~ (2000)
  9. Arthur JR, "The glutathione peroxidases", Cell Mol Life Sci, 57, pp.1825~1835 (2000)
  10. Biaglow JE, "The thioredoxin reductase", thioredoxin system : novel redox targets for cancer therapy, 2005, pp.4, 6~13
  11. Valko M, "Free radicals and antioxidants in normal physiological functions and human disease", Int J Biochem Cell Biol, 39, pp.44~84 (2007)
  12. Oguntibeju OO, "Type 2 diabetes mellitus, oxidative stress and inflammation: examining the links", Int J Physiol Pathophysiol Pharmacol, 11, pp.45~63 (2019)[DOI]
  13. Yazan Ranneh, "Crosstalk between reactive oxygen species and pro-inflammatory markers in developing various chronic diseases: a review", Applied Biological Chemistry, 60(3), pp.327~338 (2017), 한국응용생명화학회
  14. Reuter S, "Oxidative stress, inflammation, and cancer : how are they linked?", Free Radic Biol Med, 49, pp.1603~1616 (2010)
  15. Sikand G, "Top 10 dietary strategies for atherosclerotic cardiovascular risk reduction", Am J Prev Cardiol, 4, pp.100106~ (2020)
  16. He C, "Exercise-induced BCL2-regulated autophagy is required for muscle glucose homeostasis", Nature, 481, pp.511~515 (2012)
  17. Ohsumi Y, "Historical landmarks of autophagy research", Cell Res, 24, pp.9~23 (2014)
  18. Perrotta I, "Macrophage autophagy and oxidative stress : an ultrastructural and immunoelectron microscopical study", Oxid Med Cell Longev, 2011, pp.282739~ (2011)
  19. Scherz-Shouval R, "Regulation of autophagy by ROS : physiology and pathology", Trends Biochem Sci, 36, pp.30~38 (2011)
  20. Zhang Y, "Induction of autophagy is essential for monocyte-macrophage differentiation", Blood, 119, pp.2895~2905 (2012)
  21. Moore KJ, "Macrophages in the pathogenesis of atherosclerosis", Cell, 145, pp.341~355 (2011)
  22. Libby P, "Progress and challenges in translating the biology of atherosclerosis", Nature, 473, pp.317~325 (2011)
  23. Andreou DE, "Atherosclerosis : an inflammatory disease", Pharmakeftiki, 22, pp.83~96 (2009)
  24. Hansson GK, "The immune system in atherosclerosis", Nat Immunol, 12, pp.204~212 (2011)
  25. Song P, "Global and regional prevalence, burden, and risk factors for carotid atherosclerosis : a systematic review, meta-analysis, and modelling study", Lancet Glob Health, 8, pp.e721~e729 (2020)
  26. Milutinović A, "Pathogenesis of atherosclerosis in the tunica intima, media, and adventitia of coronary arteries : an updated review", Bosn J Basic Med Sci, 20, pp.21~30 (2020)
  27. Rafieian-Kopaei M, "Atherosclerosis : process, indicators, risk factors and new hopes", Int J Prev Med, 5, pp.927~946 (2014)
  28. Yang S, "Macrophage polarization in atherosclerosis", Clin Chim Acta, 501, pp.142~146 (2020)
  29. Sorokin V, "Role of vascular smooth muscle cell plasticity and interactions in vessel wall inflammation", Front Immunol, 11, pp.599415~ (2020)
  30. Doran AC, "Role of smooth muscle cells in the initiation and early progression of atherosclerosis", Arterioscler Thromb Vasc Biol, 28, pp.812~819 (2008)
  31. Khatana C, "Mechanistic insights into the oxidized low-density lipoprotein-induced atherosclerosis", Oxid Med Cell Longev, 2020, pp.5245308~ (2020)
  32. Su LJ, "Reactive oxygen species-induced lipid peroxidation in apoptosis, autophagy, and ferroptosis", Oxid Med Cell Longev, 2019, pp.5080843~ (2019)
  33. Podrez EA, "Macrophage scavenger receptor CD36 is the major receptor for LDL modified by monocyte-generated reactive nitrogen species", J Clin Invest, 105, pp.1095~1108 (2000)
  34. Kunjathoor VV, "Scavenger receptors class A-I", II and CD36 are the principal receptors responsible for the uptake of modified low density lipoprotein leading to lipid loading in macrophages, 2002, pp.277, 49982~49988
  35. Febbraio M, "Targeted disruption of the class B scavenger receptor CD36 protects against atherosclerotic lesion development in mice", J Clin Invest, 105, pp.1049~1056 (2000)
  36. Janabi M, "Oxidized LDL-induced NF-kappa B activation and subsequent expression of proinflammatory genes are defective in monocyte-derived macrophages from CD36-deficient patients", Arterioscler Thromb Vasc Biol, 20, pp.1953~1960 (2000)
  37. Park YM, "CD36 modulates migration of mouse and human macrophages in response to oxidized LDL and may contribute to macrophage trapping in the arterial intima", J Clin Invest, 119, pp.136~145 (2009)
  38. Moore KJ, "Loss of receptor-mediated lipid uptake via scavenger receptor A or CD36 pathways does not ameliorate atherosclerosis in hyperlipidemic mice", J Clin Invest, 115, pp.2192~2201 (2005)
  39. Maxeiner H, "Complementary roles for scavenger receptor A and CD36 of human monocyte-derived macrophages in adhesion to surfaces coated with oxidized low-density lipoproteins and in secretion of H2O2", J Exp Med, 188, pp.2257~2265 (1998)
  40. Allen RM, "LDL delivery of microbial small RNAs drives atherosclerosis through macrophage TLR8", Nat Cell Biol, 24, pp.1701~1713 (2022)
  41. Cokic I, "Intramyocardial hemorrhage drives fatty degeneration of infarcted myocardium", Nat Commun, 13, pp.6394~ (2022)
  42. Morris G, "Redox regulation of the immune response", Cell Mol Immunol, 19, pp.1079~1101 (2022)
  43. Khan SY, "Premature senescence of endothelial cells upon chronic exposure to TNFα can be prevented by N-acetyl cysteine and plumericin", Sci Rep, 7, pp.39501~ (2017)
  44. Ting KK, "The aging endothelium", Vasc Biol, 3, pp.R35~R47 (2021)
  45. Lozhkin A, "NADPH oxidase 4 regulates vascular inflammation in aging and atherosclerosis", J Mol Cell Cardiol, 102, pp.10~21 (2017)
  46. Chahine MN, "Oxidized LDL enhances stretch-induced smooth muscle cell proliferation through alterations in nuclear protein import", Can J Physiol Pharmacol, 90, pp.1559~1568 (2012)
  47. Peng W, "Mitochondrial dysfunction in atherosclerosis", DNA Cell Biol, 38, pp.597~606 (2019)
  48. Liu CS, "Alteration of the copy number of mitochondrial DNA in leukocytes of patients with hyperlipidemia", Ann N Y Acad Sci, 1042, pp.70~75 (2005)
  49. Esposito LA, "Mitochondrial disease in mouse results in increased oxidative stress", Proc Natl Acad Sci U S A, 96, pp.4820~4825 (1999)
  50. Chan DC, "Mitochondrial dynamics and its involvement in disease", Annu Rev Pathol, 15, pp.235~259 (2020)
  51. Madamanchi NR, "Mitochondrial dysfunction in atherosclerosis", Circ Res, 100, pp.460~473 (2007)
  52. Kinscherf R, "Induction of mitochondrial manganese superoxide dismutase in macrophages by oxidized LDL : its relevance in atherosclerosis of humans and heritable hyperlipidemic rabbits", FASEB J, 11, pp.1317~1328 (1997)
  53. Nishikawa T, "Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage", Nature, 404, pp.787~790 (2000)
  54. Wilson FH, "A cluster of metabolic defects caused by mutation in a mitochondrial tRNA", Science, 306, pp.1190~1194 (2004)
  55. Quan Y, "Mitochondrial ROS-modulated mtDNA : a potential target for cardiac aging", Oxid Med Cell Longev, 2020, pp.9423593~ (2020)
  56. Ballinger SW, "Mitochondrial integrity and function in atherogenesis", Circulation, 106, pp.544~549 (2002)
  57. Harrison CM, "Mitochondrial oxidative stress significantly influences atherogenic risk and cytokine-induced oxidant production", Environ Health Perspect, 119, pp.676~681 (2011)
  58. Ballinger SW, "Hydrogen peroxide-and peroxynitrite-induced mitochondrial DNA damage and dysfunction in vascular endothelial and smooth muscle cells", Circ Res, 86, pp.960~966 (2000)
  59. Piantadosi CA, "Mitochondrial DNA, oxidants, and innate immunity", Free Radic Biol Med, 152, pp.455~461 (2020)
  60. Cannizzo B, "Tempol attenuates atherosclerosis associated with metabolic syndrome via decreased vascular inflammation and NADPH-2 oxidase expression", Free Radic Res, 48, pp.526~533 (2014)
  61. Libby P, "Inflammation and atherosclerosis", Circulation, 105, pp.1135~1143 (2002)
  62. Hansson GK, "The immune response in atherosclerosis : a double-edged sword", Nat Rev Immunol, 6, pp.508~519 (2006)
  63. Lu N, "NLRP3-mediated inflammation in atherosclerosis and associated therapeutics", Front Cell Dev Biol, 10, pp.823387~ (2022)
  64. Kim YW, "Inflammation and oxidative stress in angiogenesis and vascular disease", J Mol Med(Berl), 91, pp.323~328 (2013)
  65. Kong P, "Inflammation and atherosclerosis : signaling pathways and therapeutic intervention", Signal Transduct Target Ther, 7, pp.131~ (2022)
  66. Hopps E, "A novel component of the metabolic syndrome : the oxidative stress", Nutr Metab Cardiovasc Dis, 20, pp.72~77 (2010)
  67. Iyer A, "Inflammatory lipid mediators in adipocyte function and obesity", Nat Rev Endocrinol, 6, pp.71~82 (2010)
  68. Leopold JA, "Oxidative risk for atherothrombotic cardiovascular disease", Free Radic Biol Med, 47, pp.1673~1706 (2009)
  69. Hussain T, "Oxidative stress and inflammation : what polyphenols can do for us?", Oxid Med Cell Longev, 2016, pp.7432797~ (2016)
  70. Sharma A, "Oxidative stress and NLRP3-inflammasome activity as significant drivers of diabetic cardiovascular complications : therapeutic implications", Front Physiol, 9, pp.114~ (2018)
  71. Duewell P, "NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals", Nature, 464, pp.1357~1361 (2010)
  72. Zheng D, "Inflammasome activation and regulation : toward a better understanding of complex mechanisms", Cell Discov, 6, pp.36~ (2020)
  73. Wang Z, "NLRP3 inflammasome and inflammatory diseases", Oxid Med Cell Longev, 2020, pp.4063562~ (2020)
  74. Heid ME, "Mitochondrial reactive oxygen species induces NLRP3-dependent lysosomal damage and inflammasome activation", J Immunol, 191, pp.5230~5238 (2013)
  75. Zhang H, "Anti-dsDNA antibodies bind to TLR4 and activate NLRP3 inflammasome in lupus monocytes", macrophages, 2016, pp.14, 156~
  76. Yang Y, "Recent advances in the mechanisms of NLRP3 inflammasome activation and its inhibitors", Cell Death Dis, 10, pp.128~ (2019)
  77. Wang R, "Activation of NLRP3 inflammasomes contributes to hyperhomocysteinemia-aggravated inflammation and atherosclerosis in ApoE-deficient mice", Lab Invest, 97, pp.922~934 (2017)
  78. Zhang X, "Use of acidic nanoparticles to rescue macrophage lysosomal dysfunction in atherosclerosis", Autophagy, 19, pp.886~903 (2023)
  79. Liu S, "HHcy induces pyroptosis and atherosclerosis via the lipid raft-mediated NOX-ROS-NLRP3 inflammasome pathway in ApoE-", -mice, 2022, pp.11, 2438~
  80. Bullón P, "Could NLRP3-inflammasome be a cardiovascular risk biomarker in acute myocardial infarction patients?", Antioxid Redox Signal, 27, pp.269~275 (2017)
  81. Sokolova M, "NLRP3 inflammasome mediates oxidative stress-induced pancreatic islet dysfunction", Am J Physiol Endocrinol Metab, 315, pp.E912~E923 (2018)
  82. Je-Wook Yu, "Mitochondria and the NLRP3 inflammasome: physiological and pathological relevance", Archives of Pharmacal Research, 39(11), pp.1503~1518 (2016), 대한약학회
  83. Brandes RP, "Vascular NADPH oxidases : molecular mechanisms of activation", Cardiovasc Res, 65, pp.16~27 (2005)
  84. Förstermann U, "Roles of vascular oxidative stress and nitric oxide in the pathogenesis of atherosclerosis", Circ Res, 120, pp.713~735 (2017)
  85. Li H, "Vascular oxidative stress, nitric oxide and atherosclerosis", Atherosclerosis, 237, pp.208~219 (2014)
  86. Patterson C, "Stimulation of a vascular smooth muscle cell NAD(P)H oxidase by thrombin. Evidence that p47(phox)may participate in forming this oxidase in vitro and in vivo", J Biol Chem, 274, pp.19814~19822 (1999)
  87. Ushio-Fukai M, "p22phox is a critical component of the superoxide-generating NADH", NADPH oxidase system and regulates angiotensin II-induced hypertrophy in vascular smooth muscle cells, 1996, pp.271, 23317~23321
  88. Hilenski LL, "Vascular medicine: a companion to Braunwald’s heart disease", pp.25~42 (2013), Saunders
  89. Park JM, "NADPH oxidase 1 mediates acute blood pressure response to angiotensin II by contributing to calcium influx in vascular smooth muscle cells", Arterioscler Thromb Vasc Biol, 42, pp.e117~ (2022)
  90. Judkins CP, "Direct evidence of a role for Nox2 in superoxide production, reduced nitric oxide bioavailability, and early atherosclerotic plaque formation in ApoE-", -mice, 2010, pp.298, H24~H32
  91. Azumi H, "Superoxide generation in directional coronary atherectomy specimens of patients with angina pectoris : important role of NAD(P)H oxidase", Arterioscler Thromb Vasc Biol, 22, pp.1838~1844 (2002)
  92. Kalinina N, "Cytochrome b558-dependent NAD(P)H oxidase-phox units in smooth muscle and macrophages of atherosclerotic lesions", Arterioscler Thromb Vasc Biol, 22, pp.2037~2043 (2002)
  93. Pandey AK, "Expression of CD70 modulates nitric oxide and redox status in endothelial cells", Arterioscler Thromb Vasc Biol, 42, pp.1169~1185 (2022)
  94. Sobenin IA, "Association of mitochondrial genetic variation with carotid atherosclerosis", PLoS One, 8, pp.e68070~ (2013)
  95. Li X, "Mitochondrial reactive oxygen species mediate lysophosphatidylcholine-induced endothelial cell activation", Arterioscler Thromb Vasc Biol, 36, pp.1090~1100 (2016)
  96. Song M, "Super-suppression of mitochondrial reactive oxygen species signaling impairs compensatory autophagy in primary mitophagic cardiomyopathy", Circ Res, 115, pp.348~353 (2014)
  97. Ming XF, "Arginase II promotes macrophage inflammatory responses through mitochondrial reactive oxygen species, contributing to insulin resistance and atherogenesis", J Am Heart Assoc, 1, pp.e000992~ (2012)
  98. Wang Y, "Macrophage mitochondrial oxidative stress promotes atherosclerosis and nuclear factor-κB-mediated inflammation in macrophages", Circ Res, 114, pp.421~433 (2014)
  99. Li J, "Electronic cigarettes induce mitochondrial DNA damage and trigger TLR9(Toll-like receptor 9)-mediated atherosclerosis", Arterioscler Thromb Vasc Biol, 41, pp.839~853 (2021)
  100. Hou Y, "CD36 promotes NLRP3 inflammasome activation via the mtROS pathway in renal tubular epithelial cells of diabetic kidneys", Cell Death Dis, 12, pp.523~ (2021)
  101. Chen ML, "Trimethylamine-N-oxide induces vascular inflammation by activating the NLRP3 inflammasome through the SIRT3-SOD2-mtROS signaling pathway", J Am Heart Assoc, 6, pp.e006347~ (2017)
  102. Usui F, "Inflammasome activation by mitochondrial oxidative stress in macrophages leads to the development of angiotensin II-induced aortic aneurysm", Arterioscler Thromb Vasc Biol, 35, pp.127~136 (2015)
  103. Nakahira K, "Autophagy proteins regulate innate immune responses by inhibiting the release of mitochondrial DNA mediated by the NALP3 inflammasome", Nat Immunol, 12, pp.222~230 (2011)
  104. Nakashima Y, "Attenuating effect of Chlorella extract on NLRP3 inflammasome activation by mitochondrial reactive oxygen species", Front Nutr, 8, pp.763492~ (2021)
  105. Taniyama Y, "Reactive oxygen species in the vasculature : molecular and cellular mechanisms", Hypertension, 42, pp.1075~1081 (2003)
  106. Cervantes Gracia K, "CVD and oxidative stress", J Clin Med, 6, pp.22~ (2017)
  107. Choi MH, "Regulation of PDGF signalling and vascular remodelling by peroxiredoxin II", Nature, 435, pp.347~353 (2005)
  108. Ouimet M, "Autophagy regulates cholesterol efflux from macrophage foam cells via lysosomal acid lipase", Cell Metab, 13, pp.655~667 (2011)
  109. Liao X, "Macrophage autophagy plays a protective role in advanced atherosclerosis", Cell Metab, 15, pp.545~553 (2012)
  110. 정세진, "The Role of Macrophage Lipophagy in Reverse Cholesterol Transport", Endocrinology and Metabolism, 32(1), pp.41~46 (2017), 대한내분비학회
  111. Emanuel R, "Induction of lysosomal biogenesis in atherosclerotic macrophages can rescue lipid-induced lysosomal dysfunction and downstream sequelae", Arterioscler Thromb Vasc Biol, 34, pp.1942~1952 (2014)
  112. Le Guezennec X, "Wip1-dependent regulation of autophagy, obesity, and atherosclerosis", Cell Metab, 16, pp.68~80 (2012)
  113. Shreeram S, "Wip1 phosphatase modulates ATM-dependent signaling pathways", Mol Cell, 23, pp.757~764 (2006)
  114. Han XB, "Upconversion nanoparticle-mediated photodynamic therapy induces autophagy and cholesterol efflux of macrophage-derived foam cells via ROS generation", Cell Death Dis, 8, pp.e2864~ (2017)
  115. Razani B, "Autophagy links inflammasomes to atherosclerotic progression", Cell Metab, 15, pp.534~544 (2012)
  116. Magné J, "ATG16L1 expression in carotid atherosclerotic plaques is associated with plaque vulnerability", Arterioscler Thromb Vasc Biol, 35, pp.1226~1235 (2015)
  117. Wang Y, "Cholesterol and bile acid-mediated regulation of autophagy in fatty liver diseases and atherosclerosis", Biochim Biophys Acta Mol Cell Biol Lipids, 1863, pp.726~733 (2018)
  118. Jeong SJ, "Prdx1(peroxiredoxin 1)deficiency reduces cholesterol efflux via impaired macrophage lipophagic flux", Autophagy, 14, pp.120~133 (2018)
  119. Shan R, "Apoptosis, autophagy and atherosclerosis : relationships and the role of Hsp27", Pharmacol Res, 166, pp.105169~ (2021)
  120. Tabas I, "Macrophage death and defective inflammation resolution in atherosclerosis", Nat Rev Immunol, 10, pp.36~46 (2010)
  121. Park JG, "Peroxiredoxin 2 deficiency exacerbates atherosclerosis in apolipoprotein E-deficient mice", Circ Res, 109, pp.739~749 (2011)
  122. Shen W, "Oxidative stress mediates chemerin-induced autophagy in endothelial cells", Free Radic Biol Med, 55, pp.73~82 (2013)
  123. Liu W, "Low shear stress inhibits endothelial mitophagy via caveolin-1", miR-7-5p, Atherosclerosis, pp.2022, 356[DOI]
  124. Bharath LP, "Impairment of autophagy in endothelial cells prevents shear-stress-induced increases in nitric oxide bioavailability", Can J Physiol Pharmacol, 92, pp.605~612 (2014)
  125. Tahrir FG, "Mitochondrial quality control in cardiac cells : mechanisms and role in cardiac cell injury and disease", J Cell Physiol, 234, pp.8122~8133 (2019)
  126. Wang Y, "MicroRNA-103 protects coronary artery endothelial cells against h2o2-induced oxidative stress via BNIP3-mediated end-stage autophagy and antipyroptosis pathways", Oxid Med Cell Longev, 2020, pp.8351342~ (2020)
  127. Takagaki Y, "Endothelial autophagy deficiency induces IL6-dependent endothelial mesenchymal transition and organ fibrosis", Autophagy, 16, pp.1905~1914 (2020)
  128. Hu M, "Substrate stiffness differentially impacts autophagy of endothelial cells and smooth muscle cells", Bioact Mater, 6, pp.1413~1422 (2020)
  129. Zhao Q, "TRPM2 promotes autophagic degradation in vascular smooth muscle cells", Sci Rep, 10, pp.20719~ (2020)
  130. Qiao L, "Deficient chaperone-mediated autophagy promotes inflammation and atherosclerosis", Circ Res, 129, pp.1141~1157 (2021)
  131. Nahapetyan H, "Mitophagy acts as a safeguard mechanism against human vascular smooth muscle cell apoptosis induced by atherogenic lipids", Atherosclerosis, 252, pp.e200~ (2016)
  132. Grootaert MO, "Defective autophagy in vascular smooth muscle cells accelerates senescence and promotes neointima formation and atherogenesis", Autophagy, 11, pp.2014~2032 (2015)
  133. Kigawa Y, "NADPH oxidase deficiency exacerbates angiotensin II-induced abdominal aortic aneurysms in mice", Arterioscler Thromb Vasc Biol, 34, pp.2413~2420 (2014)
  134. Jeong Se-Jin, "Deficiency of peroxiredoxin 2 exacerbates angiotensin II-induced abdominal aortic aneurysm", Experimental and Molecular Medicine, 52, pp.1~15 (2020), 생화학분자생물학회[DOI]
  135. Kubota Y, "Lipoprotein(a)and abdominal aortic aneurysm risk : the Atherosclerosis Risk in Communities study", Atherosclerosis, 268, pp.63~67 (2018)
  136. Li R, "EZH2 inhibits autophagic cell death of aortic vascular smooth muscle cells to affect aortic dissection", Cell Death Dis, 9, pp.180~ (2018)
  137. Osonoi Y, "Defective autophagy in vascular smooth muscle cells enhances cell death and atherosclerosis", Autophagy, 14, pp.1991~2006 (2018)
  138. Guo J, "Metformin protects against abdominal aortic aneurysm by Atg7-induced autophagy", Adv Clin Exp Med, 31, pp.59~69 (2022)
  139. Mochida A, "Defective autophagy in vascular smooth muscle cells enhances the healing of abdominal aortic aneurysm", Physiol Rep, 9, pp.e15000~ (2021)
  140. Wang Y, "Dynamic autophagic activity affected the development of thoracic aortic dissection by regulating functional properties of smooth muscle cells", Biochem Biophys Res Commun, 479, pp.358~364 (2016)
  141. Irace FG, "Role of oxidative stress and autophagy in thoracic aortic aneurysms", JACC Basic Transl Sci, 6, pp.719~730 (2021)
  142. Virani SS, "Heart Disease and Stroke Statistics-2021 update : a report from the American Heart Association", Circulation, 143, pp.e254~e743 (2021)
  143. Xie H, "Identification of featured metabolism-related genes in patients with acute myocardial infarction", Dis Markers, 2020, pp.8880004~ (2020)
  144. Yan F, "Loss of Wip1 aggravates brain injury after ischaemia", reperfusion by overactivating microglia, 2021, pp.6, 344~351
  145. Zuo W, "Mitochondria autophagy is induced after hypoxic", ischemic stress in a Drp1 dependent manner : the role of inhibition of Drp1 in ischemic brain damage, 2014, pp.86, 103~115
  146. Huang J, "The role of mitochondrial quality control in cardiac ischemia", reperfusion injury, 2021, pp.2021, 5543452~
  147. Kamada Y, "Tor-mediated induction of autophagy via an Apg1 protein kinase complex", J Cell Biol, 150, pp.1507~1513 (2000)
  148. Matsui Y, "Distinct roles of autophagy in the heart during ischemia and reperfusion : roles of AMP-activated protein kinase and Beclin 1 in mediating autophagy", Circ Res, 100, pp.914~922 (2007)
  149. Pattison JS, "Atg7 induces basal autophagy and rescues autophagic deficiency in CryABR120G cardiomyocytes", Circ Res, 109, pp.151~160 (2011)
  150. Kaizuka T, "Atg13 is essential for autophagy and cardiac development in mice", Mol Cell Biol, 36, pp.585~595 (2015)
  151. Salo PP, "Genetic variants on chromosome 1p13. 3 are associated with non-ST elevation myocardial infarction and the expression of DRAM2 in the Finnish population", PLoS One, 10, pp.e0140576~ (2015)
  152. Song E, "Cardiac autophagy deficiency attenuates ANP production and disrupts myocardial-adipose cross talk, leading to increased fat accumulation and metabolic dysfunction", Diabetes, 70, pp.51~61 (2021)
  153. Xiao C, "Transplanted mesenchymal stem cells reduce autophagic flux in infarcted hearts via the exosomal transfer of miR-125b", Circ Res, 123, pp.564~578 (2018)
  154. Ma X, "Impaired autophagosome clearance contributes to cardiomyocyte death in ischemia", reperfusion injury, 2012, pp.125, 3170~3181
  155. Qian J, "Blockade of Hsp20 phosphorylation exacerbates cardiac ischemia", reperfusion injury by suppressed autophagy and increased cell death, 2009, pp.105, 1223~1231
  156. Chen W, "Hyperbaric oxygen protects against myocardial ischemia-reperfusion injury through inhibiting mitochondria dysfunction and autophagy", Mol Med Rep, 22, pp.4254~4264 (2020)
  157. Wu D, "The role of autophagy in acute myocardial infarction", Front Pharmacol, 10, pp.551~ (2019)
  158. Sciarretta S, "Trehalose-induced activation of autophagy improves cardiac remodeling after myocardial infarction", J Am Coll Cardiol, 71, pp.1999~2010 (2018)
  159. Kanamori H, "The role of autophagy emerging in postinfarction cardiac remodelling", Cardiovasc Res, 91, pp.330~339 (2011)
  160. Kanamori H, "Autophagy limits acute myocardial infarction induced by permanent coronary artery occlusion", Am J Physiol Heart Circ Physiol, 300, pp.H2261~H2271 (2011)
  161. Maejima Y, "Mst1 inhibits autophagy by promoting the interaction between Beclin1 and Bcl-2", Nat Med, 19, pp.1478~1488 (2013)
  162. Koch JC, "The role of autophagy in axonal degeneration of the optic nerve", Exp Eye Res, 144, pp.81~89 (2016)
  163. Liton PB, "The autophagic lysosomal system in outflow pathway physiology and pathophysiology", Exp Eye Res, 144, pp.29~37 (2016)
  164. Hyman DJ, "Characteristics of patients with uncontrolled hypertension in the United States", N Engl J Med, 345, pp.479~486 (2001)
  165. NCD Risk Factor Collaboration(NCD-RisC), "Worldwide trends in hypertension prevalence and progress in treatment and control from 1990 to 2019 : a pooled analysis of 1201 population-representative studies with 104 million participants", Lancet, 398, pp.957~980 (2021)
  166. Zhu H, "Cardiac autophagy is a maladaptive response to hemodynamic stress", J Clin Invest, 117, pp.1782~1793 (2007)
  167. Nakai A, "The role of autophagy in cardiomyocytes in the basal state and in response to hemodynamic stress", Nat Med, 13, pp.619~624 (2007)
  168. Chao YM, "Redox-sensitive endoplasmic reticulum stress and autophagy at rostral ventrolateral medulla contribute to hypertension in spontaneously hypertensive rats", Hypertension, 61, pp.1270~1280 (2013)
  169. Kwon Y, "Effects of 3-methyladenine, an autophagy inhibitor, on the elevated blood pressure and arterial dysfunction of angiotensin II-induced hypertensive mice", Biomed Pharmacother, 154, pp.113588~ (2022)

관련 논문AI추천

이 간행물의 다른 논문 (9건)