Skip to main content
SpringerLink
Log in

Vascular Biology of Smooth Muscle Cells and Restenosis

  • Chapter
  • First Online:
Mechanisms of Vascular Disease

Abstract

Vascular smooth muscle cells (VSMCs) play multiple and diverse roles within the vasculature. In addition to their well-established role in regulating mechanical forces including the constriction and dilatation of blood vessels, VSMCs make significant contributions to the pathogenesis of atherosclerosis and restenosis. In atherosclerosis these include the ability to form a plaque stabilizing ‘cap’, a beneficial role. However, VSMCs may also contribute to plaque expansion through rapid proliferation when differentiated into a synthetic VSMC phenotype. VSMCs can also take up lipids and acquire inflammatory macrophage-like characteristics that further contribute to plaque growth.

Restenosis is caused by the rapid expansion of the neointima following vascular injury. It is a major complication following vascular interventions such as balloon angioplasty and stenting. VSMCs play a significant role in restenosis through multiple mechanisms including rapid dysregulated proliferation, and monocyte recruitment or differentiation into macrophages. A number of strategies have been used to prevent restenosis and new therapies are still emerging. A deeper understanding of the role of VSMCs in vascular pathologies is essential for the continued improvement of therapies that treat and prevent cardiovascular disease.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Log in via an institution
Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 84.99
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 109.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD 159.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

References

  1. Yoshida T, Owens GK. Molecular determinants of vascular smooth muscle cell diversity. Circ Res. 2005;96:280–91. https://doi.org/10.1161/01.RES.0000155951.62152.2e.

    Article  CAS  PubMed  Google Scholar 

  2. Frismantiene A, Philippova M, Erne P, Resink TJ. Smooth muscle cell-driven vascular diseases and molecular mechanisms of VSMC plasticity. Cell Signal. 2018;52:48–64. https://doi.org/10.1016/j.cellsig.2018.08.019.

    Article  CAS  PubMed  Google Scholar 

  3. Morano I. Tuning smooth muscle contraction by molecular motors. J Mol Med (Berl). 2003;81:481–7. https://doi.org/10.1007/s00109-003-0451-x.

    Article  CAS  Google Scholar 

  4. van der Vorst EP, Vanags LZ, Dunn LL, Prosser HC, Rye KA, Bursill CA. High-density lipoproteins suppress chemokine expression and proliferation in human vascular smooth muscle cells. FASEB J. 2013;27:1413–25. https://doi.org/10.1096/fj.12-212753.

    Article  CAS  PubMed  Google Scholar 

  5. Bennett MR, Sinha S, Owens GK. Vascular smooth muscle cells in atherosclerosis. Circ Res. 2016;118:692–702. https://doi.org/10.1161/CIRCRESAHA.115.306361.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  6. Weber C, Noels H. Atherosclerosis: current pathogenesis and therapeutic options. Nat Med. 2011;17:1410–22. https://doi.org/10.1038/nm.2538.

    Article  CAS  PubMed  Google Scholar 

  7. Bauriedel G, Hutter R, Welsch U, Bach R, Sievert H, Luderitz B. Role of smooth muscle cell death in advanced coronary primary lesions: implications for plaque instability. Cardiovasc Res. 1999;41:480–8. https://doi.org/10.1016/s0008-6363(98)00318-6.

    Article  CAS  PubMed  Google Scholar 

  8. Chang SF, Chen LJ, Lee PL, Lee DY, Chien S, Chiu JJ. Different modes of endothelial-smooth muscle cell interaction elicit differential beta-catenin phosphorylations and endothelial functions. Proc Natl Acad Sci U S A. 2014;111:1855–60. https://doi.org/10.1073/pnas.1323761111.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  9. Doran AC, Meller N, McNamara CA. Role of smooth muscle cells in the initiation and early progression of atherosclerosis. Arterioscler Thromb Vasc Biol. 2008;28:812–9. https://doi.org/10.1161/ATVBAHA.107.159327.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  10. Lucas AD, Bursill C, Guzik TJ, Sadowski J, Channon KM, Greaves DR. Smooth muscle cells in human atherosclerotic plaques express the fractalkine receptor CX3CR1 and undergo chemotaxis to the CX3C chemokine fractalkine (CX3CL1). Circulation. 2003;108:2498–504.

    Article  CAS  Google Scholar 

  11. Barlic JZY, Foley JF, Murphy PM. Oxidized lipid-driven chemokine receptor switch, CCR2 to CX3CR1, mediates adhesion of human macrophages to coronary artery smooth muscle cells through a peroxisome proliferator-activated receptor gamma-dependent pathway. Circulation. 2006;114(8):807–19.

    Article  CAS  Google Scholar 

  12. Bennett MR, Evan GI, Schwartz SM. Apoptosis of human vascular smooth muscle cells derived from normal vessels and coronary atherosclerotic plaques. J Clin Invest. 1995;95:2266–74. https://doi.org/10.1172/JCI117917.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  13. Boyle JJ, Weissberg PL, Bennett MR. Human macrophage-induced vascular smooth muscle cell apoptosis requires NO enhancement of Fas/Fas-L interactions. Arterioscler Thromb Vasc Biol. 2002;22:1624–30.

    Article  CAS  Google Scholar 

  14. Clarke MC, Talib S, Figg NL, Bennett MR. Vascular smooth muscle cell apoptosis induces interleukin-1-directed inflammation: effects of hyperlipidemia-mediated inhibition of phagocytosis. Circ Res. 2010;106:363–72. https://doi.org/10.1161/CIRCRESAHA.109.208389.

    Article  CAS  PubMed  Google Scholar 

  15. Zhang L, Issa Bhaloo S, Chen T, Zhou B, Xu Q. Role of resident stem cells in vessel formation and arteriosclerosis. Circ Res. 2018;122:1608–24. https://doi.org/10.1161/CIRCRESAHA.118.313058.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  16. Trigueros-Motos L, Gonzalez-Granado JM, Cheung C, Fernandez P, Sanchez-Cabo F, Dopazo A, et al. Embryological-origin-dependent differences in homeobox expression in adult aorta: role in regional phenotypic variability and regulation of NF-kappaB activity. Arterioscler Thromb Vasc Biol. 2013;33:1248–56. https://doi.org/10.1161/ATVBAHA.112.300539.

    Article  CAS  PubMed  Google Scholar 

  17. Dalton ML, Gadson PF Jr, Wrenn RW, Rosenquist TH. Homocysteine signal cascade: production of phospholipids, activation of protein kinase C, and the induction of c-fos and c-myb in smooth muscle cells. FASEB J. 1997;11:703–11. https://doi.org/10.1096/fasebj.11.8.9240971.

    Article  CAS  PubMed  Google Scholar 

  18. Leroux-Berger M, Queguiner I, Maciel TT, Ho A, Relaix F, Kempf H. Pathologic calcification of adult vascular smooth muscle cells differs on their crest or mesodermal embryonic origin. J Bone Miner Res. 2011;26:1543–53. https://doi.org/10.1002/jbmr.382.

    Article  CAS  PubMed  Google Scholar 

  19. Allahverdian S, Chaabane C, Boukais K, Francis GA, Bochaton-Piallat ML. Smooth muscle cell fate and plasticity in atherosclerosis. Cardiovasc Res. 2018;114:540–50. https://doi.org/10.1093/cvr/cvy022.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  20. Owens GK, Kumar MS, Wamhoff BR. Molecular regulation of vascular smooth muscle cell differentiation in development and disease. Physiol Rev. 2004;84:767–801. https://doi.org/10.1152/physrev.00041.2003.

    Article  CAS  PubMed  Google Scholar 

  21. Shankman LS, Gomez D, Cherepanova OA, Salmon M, Alencar GF, Haskins RM, et al. KLF4-dependent phenotypic modulation of smooth muscle cells has a key role in atherosclerotic plaque pathogenesis. Nat Med. 2015;21:628–37. https://doi.org/10.1038/nm.3866.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  22. Feil S, Fehrenbacher B, Lukowski R, Essmann F, Schulze-Osthoff K, Schaller M, et al. Transdifferentiation of vascular smooth muscle cells to macrophage-like cells during atherogenesis. Circ Res. 2014;115:662–7. https://doi.org/10.1161/CIRCRESAHA.115.304634.

    Article  CAS  PubMed  Google Scholar 

  23. Ackers-Johnson M, Talasila A, Sage AP, Long X, Bot I, Morrell NW, et al. Myocardin regulates vascular smooth muscle cell inflammatory activation and disease. Arterioscler Thromb Vasc Biol. 2015;35:817–28. https://doi.org/10.1161/ATVBAHA.114.305218.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  24. Alexander MR, Murgai M, Moehle CW, Owens GK. Interleukin-1beta modulates smooth muscle cell phenotype to a distinct inflammatory state relative to PDGF-DD via NF-kappaB-dependent mechanisms. Physiol Genomics. 2012;44:417–29. https://doi.org/10.1152/physiolgenomics.00160.2011.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  25. Yoshida T, Kaestner KH, Owens GK. Conditional deletion of Kruppel-like factor 4 delays downregulation of smooth muscle cell differentiation markers but accelerates neointimal formation following vascular injury. Circ Res. 2008;102:1548–57. https://doi.org/10.1161/CIRCRESAHA.108.176974.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  26. Rong JX, Shapiro M, Trogan E, Fisher EA. Transdifferentiation of mouse aortic smooth muscle cells to a macrophage-like state after cholesterol loading. Proc Natl Acad Sci U S A. 2003;100:13531–6.

    Article  CAS  Google Scholar 

  27. Vengrenyuk Y, Nishi H, Long X, Ouimet M, Savji N, Martinez FO, et al. Cholesterol loading reprograms the microRNA-143/145-myocardin axis to convert aortic smooth muscle cells to a dysfunctional macrophage-like phenotype. Arterioscler Thromb Vasc Biol. 2015;35:535–46. https://doi.org/10.1161/ATVBAHA.114.304029.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  28. Tsai TN, Kirton JP, Campagnolo P, Zhang L, Xiao Q, Zhang Z, et al. Contribution of stem cells to neointimal formation of decellularized vessel grafts in a novel mouse model. Am J Pathol. 2012;181:362–73. https://doi.org/10.1016/j.ajpath.2012.03.021.

    Article  CAS  PubMed  Google Scholar 

  29. Hu Y, Zhang Z, Torsney E, Afzal AR, Davison F, Metzler B, et al. Abundant progenitor cells in the adventitia contribute to atherosclerosis of vein grafts in ApoE-deficient mice. J Clin Invest. 2004;113:1258–65. https://doi.org/10.1172/JCI19628.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  30. Zernecke A, Schober A, Bot I, von Hundelshausen P, Liehn EA, Mopps B, et al. SDF-1alpha/CXCR4 axis is instrumental in neointimal hyperplasia and recruitment of smooth muscle progenitor cells. Circ Res. 2005;96:784–91. https://doi.org/10.1161/01.RES.0000162100.52009.38.

    Article  CAS  PubMed  Google Scholar 

  31. Perlman H, Maillard L, Krasinski K, Walsh K. Evidence for the rapid onset of apoptosis in medial smooth muscle cells after balloon injury. Circulation. 1997;95:981–7.

    Article  CAS  Google Scholar 

  32. van Beusekom HM, Whelan DM, Hofma SH, Krabbendam SC, van Hinsbergh VW, Verdouw PD, et al. Long-term endothelial dysfunction is more pronounced after stenting than after balloon angioplasty in porcine coronary arteries. J Am Coll Cardiol. 1998;32:1109–17.

    Article  Google Scholar 

  33. Caramori PR, Lima VC, Seidelin PH, Newton GE, Parker JD, Adelman AG. Long-term endothelial dysfunction after coronary artery stenting. J Am Coll Cardiol. 1999;34:1675–9.

    Article  CAS  Google Scholar 

  34. Swanson N, Hogrefe K, Javed Q, Malik N, Gershlick AH. Vascular endothelial growth factor (VEGF)-eluting stents: in vivo effects on thrombosis, endothelialization and intimal hyperplasia. J Invasive Cardiol. 2003;15:688–92.

    PubMed  Google Scholar 

  35. Selzman CH, Miller SA, Zimmerman MA, Gamboni-Robertson F, Harken AH, Banerjee A. Monocyte chemotactic protein-1 directly induces human vascular smooth muscle proliferation. Am J Physiol Heart Circ Physiol. 2002;283:H1455–61. https://doi.org/10.1152/ajpheart.00188.2002.

    Article  CAS  PubMed  Google Scholar 

  36. Kovacic JC, Gupta R, Lee AC, Ma M, Fang F, Tolbert CN, et al. Stat3-dependent acute Rantes production in vascular smooth muscle cells modulates inflammation following arterial injury in mice. J Clin Invest. 2010;120:303–14. https://doi.org/10.1172/JCI40364.

    Article  CAS  PubMed  Google Scholar 

  37. Chandrasekar B, Mummidi S, Perla RP, Bysani S, Dulin NO, Liu F, et al. Fractalkine (CX3CL1) stimulated by nuclear factor kappaB (NF-kappaB)-dependent inflammatory signals induces aortic smooth muscle cell proliferation through an autocrine pathway. Biochem J. 2003;373:547–58.

    Article  CAS  Google Scholar 

  38. Schober A, Zernecke A, Liehn EA, von Hundelshausen P, Knarren S, Kuziel WA, et al. Crucial role of the CCL2/CCR2 axis in neointimal hyperplasia after arterial injury in hyperlipidemic mice involves early monocyte recruitment and CCL2 presentation on platelets. Circ Res. 2004;95:1125–33. https://doi.org/10.1161/01.RES.0000149518.86865.3e.

    Article  CAS  PubMed  Google Scholar 

  39. Zimmerman MA, Selzman CH, Reznikov LL, Miller SA, Raeburn CD, Emmick J, et al. Lack of TNF-alpha attenuates intimal hyperplasia after mouse carotid artery injury. Am J Physiol Regul Integr Comp Physiol. 2002;283:R505–12. https://doi.org/10.1152/ajpregu.00033.2002.

    Article  CAS  PubMed  Google Scholar 

  40. Wilson DP. Vascular smooth muscle structure and function. In: Fitridge R, Thompson M, editors. Mechanisms of vascular disease: a reference book for vascular specialists. Adelaide: University of Adelaide Press; 2011.

    Google Scholar 

  41. Zhou M, Sutliff RL, Paul RJ, Lorenz JN, Hoying JB, Haudenschild CC, et al. Fibroblast growth factor 2 control of vascular tone. Nat Med. 1998;4:201–7.

    Article  CAS  Google Scholar 

  42. Zimmerman MA, Selzman CH, Reznikov LL, Raeburn CD, Barsness K, McIntyre RC Jr, et al. Interleukin-11 attenuates human vascular smooth muscle cell proliferation. Am J Physiol Heart Circ Physiol. 2002;283:H175–80. https://doi.org/10.1152/ajpheart.00987.2001.

    Article  CAS  PubMed  Google Scholar 

  43. Chung IM, Gold HK, Schwartz SM, Ikari Y, Reidy MA, Wight TN. Enhanced extracellular matrix accumulation in restenosis of coronary arteries after stent deployment. J Am Coll Cardiol. 2002;40:2072–81.

    Article  CAS  Google Scholar 

  44. Shimizu-Hirota R, Sasamura H, Kuroda M, Kobayashi E, Hayashi M, Saruta T. Extracellular matrix glycoprotein biglycan enhances vascular smooth muscle cell proliferation and migration. Circ Res. 2004;94:1067–74. https://doi.org/10.1161/01.RES.0000126049.79800.CA.

    Article  CAS  PubMed  Google Scholar 

  45. Bauters C, Meurice T, Hamon M, McFadden E, Lablanche JM, Bertrand ME. Mechanisms and prevention of restenosis: from experimental models to clinical practice. Cardiovasc Res. 1996;31:835–46.

    Article  CAS  Google Scholar 

  46. Wong CS, Leon MB, Popma JJ. New device angioplasty: the impact on restenosis. Coron Artery Dis. 1993;4:243–53.

    Article  CAS  Google Scholar 

  47. Inoue T, Croce K, Morooka T, Sakuma M, Node K, Simon DI. Vascular inflammation and repair: implications for re-endothelialization, restenosis, and stent thrombosis. JACC Cardiovasc Interv. 2011;4:1057–66. https://doi.org/10.1016/j.jcin.2011.05.025.

    Article  PubMed  PubMed Central  Google Scholar 

  48. Leon MB, Baim DS, Popma JJ, Gordon PC, Cutlip DE, Ho KK, et al. A clinical trial comparing three antithrombotic-drug regimens after coronary-artery stenting. Stent anticoagulation restenosis study investigators. N Engl J Med. 1998;339:1665–71. https://doi.org/10.1056/NEJM199812033392303.

    Article  CAS  PubMed  Google Scholar 

  49. Berger PB, Kleiman NS, Pencina MJ, Hsieh WH, Steinhubl SR, Jeremias A, et al. Frequency of major noncardiac surgery and subsequent adverse events in the year after drug-eluting stent placement results from the EVENT (evaluation of drug-eluting stents and ischemic events) registry. JACC Cardiovasc Interv. 2010;3:920–7. https://doi.org/10.1016/j.jcin.2010.03.021.

    Article  PubMed  Google Scholar 

  50. Fukuyama J, Ichikawa K, Hamano S, Shibata N. Tranilast suppresses the vascular intimal hyperplasia after balloon injury in rabbits fed on a high-cholesterol diet. Eur J Pharmacol. 1996;318:327–32. https://doi.org/10.1016/s0014-2999(96)00774-1.

    Article  CAS  PubMed  Google Scholar 

  51. Ishiwata S, Verheye S, Robinson KA, Salame MY, de Leon H, King SB 3rd, et al. Inhibition of neointima formation by tranilast in pig coronary arteries after balloon angioplasty and stent implantation. J Am Coll Cardiol. 2000;35:1331–7.

    Article  CAS  Google Scholar 

  52. Holmes DR Jr, Savage M, LaBlanche JM, Grip L, Serruys PW, Fitzgerald P, et al. Results of prevention of REStenosis with Tranilast and its outcomes (PRESTO) trial. Circulation. 2002;106:1243–50. https://doi.org/10.1161/01.cir.0000028335.31300.da.

    Article  PubMed  Google Scholar 

  53. Wessely R, Schomig A, Kastrati A. Sirolimus and paclitaxel on polymer-based drug-eluting stents: similar but different. J Am Coll Cardiol. 2006;47:708–14. https://doi.org/10.1016/j.jacc.2005.09.047.

    Article  CAS  PubMed  Google Scholar 

  54. Morice MC, Serruys PW, Sousa JE, Fajadet J, Ban Hayashi E, Perin M, et al. A randomized comparison of a sirolimus-eluting stent with a standard stent for coronary revascularization. N Engl J Med. 2002;346:1773–80. https://doi.org/10.1056/NEJMoa012843.

    Article  CAS  PubMed  Google Scholar 

  55. Park SJ, Park DW, Kim YH, Kang SJ, Lee SW, Lee CW, et al. Duration of dual antiplatelet therapy after implantation of drug-eluting stents. N Engl J Med. 2010;362:1374–82. https://doi.org/10.1056/NEJMoa1001266.

    Article  CAS  PubMed  Google Scholar 

  56. Daemen J, Wenaweser P, Tsuchida K, Abrecht L, Vaina S, Morger C, et al. Early and late coronary stent thrombosis of sirolimus-eluting and paclitaxel-eluting stents in routine clinical practice: data from a large two-institutional cohort study. Lancet. 2007;369:667–78. https://doi.org/10.1016/S0140-6736(07)60314-6.

    Article  CAS  PubMed  Google Scholar 

  57. Gareri C, De Rosa S, Indolfi C. MicroRNAs for restenosis and thrombosis after vascular injury. Circ Res. 2016;118:1170–84. https://doi.org/10.1161/CIRCRESAHA.115.308237.

    Article  CAS  PubMed  Google Scholar 

  58. Wang D, Deuse T, Stubbendorff M, Chernogubova E, Erben RG, Eken SM, et al. Local MicroRNA modulation using a novel anti-miR-21-eluting stent effectively prevents experimental in-stent restenosis. Arterioscler Thromb Vasc Biol. 2015;35:1945–53. https://doi.org/10.1161/ATVBAHA.115.305597.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  59. Zhang B, Yao Y, Sun QF, Liu SQ, Jing B, Yuan C, et al. Circulating mircoRNA-21 as a predictor for vascular restenosis after interventional therapy in patients with lower extremity arterial occlusive disease. Biosci Rep. 2017;37. https://doi.org/10.1042/BSR20160502.

  60. Zhu ZR, He Q, Wu WB, Chang GQ, Yao C, Zhao Y, et al. MiR-140-3p is involved in in-stent restenosis by targeting C-Myb and BCL-2 in peripheral artery disease. J Atheroscler Thromb. 2018;25:1168–81. https://doi.org/10.5551/jat.44024.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  61. Gareri C, Iaconetti C, Sorrentino S, Covello C, De Rosa S, Indolfi C. miR-125a-5p modulates phenotypic switch of vascular smooth muscle cells by targeting ETS-1. J Mol Biol. 2017;429:1817–28. https://doi.org/10.1016/j.jmb.2017.05.008.

    Article  CAS  PubMed  Google Scholar 

  62. Chen C, Yan Y, Liu X. microRNA-612 is downregulated by platelet-derived growth factor-BB treatment and has inhibitory effects on vascular smooth muscle cell proliferation and migration via directly targeting AKT2. Exp Ther Med. 2018;15:159–65. https://doi.org/10.3892/etm.2017.5428.

    Article  CAS  PubMed  Google Scholar 

  63. Izuhara M, Kuwabara Y, Saito N, Yamamoto E, Hakuno D, Nakashima Y, et al. Prevention of neointimal formation using miRNA-126-containing nanoparticle-conjugated stents in a rabbit model. PLoS One. 2017;12:e0172798. https://doi.org/10.1371/journal.pone.0172798.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  64. Welten SMJ, de Jong RCM, Wezel A, de Vries MR, Boonstra MC, Parma L, et al. Inhibition of 14q32 microRNA miR-495 reduces lesion formation, intimal hyperplasia and plasma cholesterol levels in experimental restenosis. Atherosclerosis. 2017;261:26–36. https://doi.org/10.1016/j.atherosclerosis.2017.04.011.

    Article  CAS  PubMed  Google Scholar 

  65. Yuan L, Dong J, Zhu G, Bao J, Lu Q, Zhou J, et al. Diagnostic value of circulating microRNAs for in-stent restenosis in patients with lower extremity arterial occlusive disease. Sci Rep. 2019;9:1402. https://doi.org/10.1038/s41598-018-36295-2.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  66. Stojkovic S, Jurisic M, Kopp CW, Koppensteiner R, Huber K, Wojta J, et al. Circulating microRNAs identify patients at increased risk of in-stent restenosis after peripheral angioplasty with stent implantation. Atherosclerosis. 2018;269:197–203. https://doi.org/10.1016/j.atherosclerosis.2018.01.020.

    Article  CAS  PubMed  Google Scholar 

  67. O’Sullivan JF, Neylon A, Fahy EF, Yang P, McGorrian C, Blake GJ. MiR-93-5p is a novel predictor of coronary in-stent restenosis. Heart Asia. 2019;11:e011134. https://doi.org/10.1136/heartasia-2018-011134.

    Article  PubMed  PubMed Central  Google Scholar 

  68. Romero ME, Yahagi K, Kolodgie FD, Virmani R. Neoatherosclerosis from a pathologist’s point of view. Arterioscler Thromb Vasc Biol. 2015;35:e43–9. https://doi.org/10.1161/ATVBAHA.115.306251.

    Article  CAS  PubMed  Google Scholar 

  69. Nakazawa G, Otsuka F, Nakano M, Vorpahl M, Yazdani SK, Ladich E, et al. The pathology of neoatherosclerosis in human coronary implants bare-metal and drug-eluting stents. J Am Coll Cardiol. 2011;57:1314–22. https://doi.org/10.1016/j.jacc.2011.01.011.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  70. Taniwaki M, Windecker S, Zaugg S, Stefanini GG, Baumgartner S, Zanchin T, et al. The association between in-stent neoatherosclerosis and native coronary artery disease progression: a long-term angiographic and optical coherence tomography cohort study. Eur Heart J. 2015;36:2167–76. https://doi.org/10.1093/eurheartj/ehv227.

    Article  PubMed  Google Scholar 

Further Reading

Download references

Author information

Authors and Affiliations

  1. Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, SA, Australia

    Victoria Nankivell, Khalia Primer, Achini Vidanapathirana, Peter Psaltis & Christina Bursill

  2. Vascular Research Centre, Lifelong Health Theme, South Australian Health and Medical Research Institute, Adelaide, SA, Australia

    Victoria Nankivell, Khalia Primer, Achini Vidanapathirana, Peter Psaltis & Christina Bursill

Authors
  1. Victoria Nankivell
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Khalia Primer
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Achini Vidanapathirana
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Peter Psaltis
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Christina Bursill
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Christina Bursill .

Editor information

Editors and Affiliations

  1. Discipline of Surgery, The University of Adelaide, Adelaide, SA, Australia

    Robert Fitridge

Rights and permissions

Reprints and permissions

Copyright information

© 2020 Springer Nature Switzerland AG

About this chapter

Check for updates. Verify currency and authenticity via CrossMark

Cite this chapter

Nankivell, V., Primer, K., Vidanapathirana, A., Psaltis, P., Bursill, C. (2020). Vascular Biology of Smooth Muscle Cells and Restenosis. In: Fitridge, R. (eds) Mechanisms of Vascular Disease. Springer, Cham. https://doi.org/10.1007/978-3-030-43683-4_6

Download citation

  • DOI: https://doi.org/10.1007/978-3-030-43683-4_6

  • Published:

  • Publisher Name: Springer, Cham

  • Print ISBN: 978-3-030-43682-7

  • Online ISBN: 978-3-030-43683-4

  • eBook Packages: MedicineMedicine (R0)

Publish with us

Policies and ethics

Search

Navigation