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Vascular aging: insights from studies on cellular senescence, stem cell aging, and progeroid syndromes

Nature Clinical Practice Cardiovascular Medicine volume 5, pages 637–648 (2008)Cite this article

Abstract

Epidemiological studies have shown that age is the chief risk factor for atherosclerotic cardiovascular diseases, but the molecular mechanisms that underlie the increase in risk conferred by aging remain unclear. Evidence suggests that the cardiovascular repair system is impaired with advancing age, thereby inducing age-associated cardiovascular dysfunction. Such impairment could be attributable to senescence of cardiovascular tissues at the cellular level as a result of telomere shortening, DNA damage, and genomic instability. In fact, the replicative ability of cardiovascular cells, particularly stem cells and/or progenitor cells, has been shown to decline with age. Recently, considerable progress has been made in understanding the pathogenesis of human progeroid syndromes that feature cardiovascular aging. Most of the genes responsible have a role in DNA metabolism, and mutated forms of these genes result in alterations of the response to DNA damage and in decreased cell proliferation, which might be common features of a phenotype of aging. Here we review the cardiovascular research on cellular senescence, stem cell aging, and progeroid syndromes and discuss the potential role of cellular senescence in the mechanisms underlying both normal aging and premature aging syndromes.

Key Points

  • Cellular senescence probably contributes to the pathogenesis of cardiovascular disease

  • Telomere integrity is impaired with advancing age, which leads to vascular dysfunction

  • The number and function of cardiovascular stem cells and/or progenitor cells shows a progressive decline with age

  • Telomere attrition, DNA damage, and genomic instability might be common features of both normal aging and progeroid syndromes

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Figure 1: Telomeres and telomerase.
Figure 2: Endothelial repair.
Figure 3: Histological features of progeroid vascular tissues.
Figure 4: Potential common pathways for normal aging and age-associated cardiovascular disease.

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References

  1. Lakatta EG and Levy D (2003) Arterial and cardiac aging: major shareholders in cardiovascular disease enterprises: Part I: aging arteries: a “set up” for vascular disease. Circulation 107: 139–146

    Article  PubMed  Google Scholar 

  2. Lakatta EG (2003) Arterial and cardiac aging: major shareholders in cardiovascular disease enterprises: Part III: cellular and molecular clues to heart and arterial aging. Circulation 107: 490–497

    Article  PubMed  Google Scholar 

  3. Reed MJ and Edelberg JM (2004) Impaired angiogenesis in the aged. Sci Aging Knowledge Environ 7: pe7

    Google Scholar 

  4. Gennaro G et al. (2003) Age-dependent impairment of reendothelialization after arterial injury: role of vascular endothelial growth factor. Circulation 107: 230–233

    Article  PubMed  Google Scholar 

  5. Minamino T and Komuro I (2007) Vascular cell senescence: contribution to atherosclerosis. Circ Res 100: 15–26

    Article  CAS  PubMed  Google Scholar 

  6. Ballard VL and Edelberg JM (2007) Stem cells and the regeneration of the aging cardiovascular system. Circ Res 100: 1116–1127

    Article  CAS  PubMed  Google Scholar 

  7. Thompson KV and Holliday R (1983) Genetic effects on the longevity of cultured human fibroblasts: II. DNA repair deficient syndromes. Gerontology 29: 83–88

    Article  CAS  PubMed  Google Scholar 

  8. Burrig KF (1991) The endothelium of advanced arteriosclerotic plaques in humans. Arterioscler Thromb 11: 1678–1689

    Article  CAS  PubMed  Google Scholar 

  9. Ross R et al. (1984) Human atherosclerosis: I. cell constitution and characteristics of advanced lesions of the superficial femoral artery. Am J Pathol 114: 79–93

    CAS  PubMed  PubMed Central  Google Scholar 

  10. Minamino T et al. (2002) Endothelial cell senescence in human atherosclerosis: role of telomere in endothelial dysfunction. Circulation 105: 1541–1544

    Article  CAS  PubMed  Google Scholar 

  11. Minamino T et al. (2003) Ras induces vascular smooth muscle cell senescence and inflammation in human atherosclerosis. Circulation 108: 2264–2269

    Article  CAS  PubMed  Google Scholar 

  12. Blasco MA (2005) Telomeres and human disease: ageing, cancer and beyond. Nat Rev Genet 6: 611–622

    Article  CAS  PubMed  Google Scholar 

  13. Herbig U et al. (2004) Telomere shortening triggers senescence of human cells through a pathway involving ATM, p53, and p21(CIP1), but not p16(INK4a). Mol Cell 14: 501–513

    Article  CAS  PubMed  Google Scholar 

  14. d'Adda di Fagagna F et al. (2003) A DNA damage checkpoint response in telomere-initiated senescence. Nature 426: 194–198

    Article  CAS  PubMed  Google Scholar 

  15. Takai H et al. (2003) DNA damage foci at dysfunctional telomeres. Curr Biol 13: 1549–1556

    Article  CAS  PubMed  Google Scholar 

  16. Herbig U et al. (2006) Cellular senescence in aging primates. Science 311: 1257

    Article  CAS  PubMed  Google Scholar 

  17. Chang E and Harley CB (1995) Telomere length and replicative aging in human vascular tissues. Proc Natl Acad Sci USA 92: 11190–11194

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  18. Aviv H et al. (2001) Age dependent aneuploidy and telomere length of the human vascular endothelium. Atherosclerosis 159: 281–287

    Article  CAS  PubMed  Google Scholar 

  19. Ogami M et al. (2004) Telomere shortening in human coronary artery diseases. Arterioscler Thromb Vasc Biol 24: 546–550

    Article  CAS  PubMed  Google Scholar 

  20. Voghel G et al. (2007) Cellular senescence in endothelial cells from atherosclerotic patients is accelerated by oxidative stress associated with cardiovascular risk factors. Mech Ageing Dev 128: 662–671

    Article  CAS  PubMed  Google Scholar 

  21. Minamino T and Kourembanas S (2001) Mechanisms of telomerase induction during vascular smooth muscle cell proliferation. Circ Res 89: 237–243

    Article  CAS  PubMed  Google Scholar 

  22. Minamino T et al. (2001) Hypoxia extends the life span of vascular smooth muscle cells through telomerase activation. Mol Cell Biol 21: 3336–3342

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  23. Matsushita H et al. (2001) eNOS activity is reduced in senescent human endothelial cells: preservation by hTERT immortalization. Circ Res 89: 793–798

    Article  CAS  PubMed  Google Scholar 

  24. Yang J et al. (1999) Human endothelial cell life extension by telomerase expression. J Biol Chem 274: 26141–26148

    Article  CAS  PubMed  Google Scholar 

  25. Yang J et al. (2001) Telomerized human microvasculature is functional in vivo. Nat Biotechnol 19: 219–224

    Article  CAS  PubMed  Google Scholar 

  26. Blasco MA et al. (1997) Telomere shortening and tumor formation by mouse cells lacking telomerase RNA. Cell 91: 25–34

    Article  CAS  PubMed  Google Scholar 

  27. Lee HW et al. (1998) Essential role of mouse telomerase in highly proliferative organs. Nature 392: 569–574

    Article  CAS  PubMed  Google Scholar 

  28. Rudolph KL et al. (1999) Longevity, stress response, and cancer in aging telomerase-deficient mice. Cell 96: 701–712

    Article  CAS  PubMed  Google Scholar 

  29. Franco S et al. (2002) Decreased B16F10 melanoma growth and impaired vascularization in telomerase-deficient mice with critically short telomeres. Cancer Res 62: 552–559

    CAS  PubMed  Google Scholar 

  30. Poch E et al. (2004) Short telomeres protect from diet-induced atherosclerosis in apolipoprotein E-null mice. FASEB J 18: 418–420

    Article  CAS  PubMed  Google Scholar 

  31. Perez-Rivero G et al. (2006) Mice deficient in telomerase activity develop hypertension because of an excess of endothelin production. Circulation 114: 309–317

    Article  CAS  PubMed  Google Scholar 

  32. Najjar SS et al. (2005) Arterial aging: is it an immutable cardiovascular risk factor? Hypertension 46: 454–462

    Article  CAS  PubMed  Google Scholar 

  33. Kunieda T et al. (2006) Angiotensin II induces premature senescence of vascular smooth muscle cells and accelerates the development of atherosclerosis via a p21-dependent pathway. Circulation 114: 953–960

    Article  CAS  PubMed  Google Scholar 

  34. Matthews C et al. (2006) Vascular smooth muscle cells undergo telomere-based senescence in human atherosclerosis: effects of telomerase and oxidative stress. Circ Res 99: 156–164

    Article  CAS  PubMed  Google Scholar 

  35. Kurz DJ et al. (2004) Chronic oxidative stress compromises telomere integrity and accelerates the onset of senescence in human endothelial cells. J Cell Sci 117: 2417–2426

    Article  CAS  PubMed  Google Scholar 

  36. Voghel G et al. (2008) Chronic treatment with N-acetyl-cystein delays cellular senescence in endothelial cells isolated from a subgroup of atherosclerotic patients. Mech Ageing Dev 129: 261–270

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  37. Hasty P et al. (2003) Aging and genome maintenance: lessons from the mouse? Science 299: 1355–1359

    Article  CAS  PubMed  Google Scholar 

  38. Tyner SD et al. (2002) p53 mutant mice that display early ageing-associated phenotypes. Nature 415: 45–53

    Article  CAS  PubMed  Google Scholar 

  39. Maier B et al. (2004) Modulation of mammalian life span by the short isoform of p53. Genes Dev 18: 306–319

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  40. Cao L et al. (2003) Senescence, aging, and malignant transformation mediated by p53 in mice lacking the Brca1 full-length isoform. Genes Dev 17: 201–213

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  41. Asahara T et al. (1997) Isolation of putative progenitor endothelial cells for angiogenesis. Science 275: 964–967

    Article  CAS  PubMed  Google Scholar 

  42. Shi Q et al. (1998) Evidence for circulating bone marrow-derived endothelial cells. Blood 92: 362–367

    Article  CAS  PubMed  Google Scholar 

  43. Rafii S and Lyden D (2003) Therapeutic stem and progenitor cell transplantation for organ vascularization and regeneration. Nat Med 9: 702–712

    Article  CAS  PubMed  Google Scholar 

  44. Walter DH et al. (2002) Statin therapy accelerates reendothelialization: a novel effect involving mobilization and incorporation of bone marrow-derived endothelial progenitor cells. Circulation 105: 3017–3024

    Article  CAS  PubMed  Google Scholar 

  45. Purhonen S et al. (2008) Bone marrow-derived circulating endothelial precursors do not contribute to vascular endothelium and are not needed for tumor growth. Proc Natl Acad Sci USA 105: 6620–6625

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  46. Thum T et al. (2007) Age-dependent impairment of endothelial progenitor cells is corrected by growth-hormone-mediated increase of insulin-like growth-factor-1. Circ Res 100: 434–443

    Article  CAS  PubMed  Google Scholar 

  47. Vasa M et al. (2001) Number and migratory activity of circulating endothelial progenitor cells inversely correlate with risk factors for coronary artery disease. Circ Res 89: E1–E7

    Article  CAS  PubMed  Google Scholar 

  48. Scheubel RJ et al. (2003) Age-dependent depression in circulating endothelial progenitor cells in patients undergoing coronary artery bypass grafting. J Am Coll Cardiol 42: 2073–2080

    Article  PubMed  Google Scholar 

  49. Hill JM et al. (2003) Circulating endothelial progenitor cells, vascular function, and cardiovascular risk. N Engl J Med 348: 593–600

    Article  PubMed  Google Scholar 

  50. Sugihara S et al. (2007) Age-related BM-MNC dysfunction hampers neovascularization. Mech Ageing Dev 128: 511–516

    Article  CAS  PubMed  Google Scholar 

  51. Heeschen C et al. (2004) Profoundly reduced neovascularization capacity of bone marrow mononuclear cells derived from patients with chronic ischemic heart disease. Circulation 109: 1615–1622

    Article  PubMed  Google Scholar 

  52. Ward M R et al. (2007) Endothelial progenitor cell therapy for the treatment of coronary disease, acute MI, and pulmonary arterial hypertension: current perspectives. Catheter Cardiovasc Interv 70: 983–998

    Article  PubMed  Google Scholar 

  53. Edelberg JM et al. (2002) Young adult bone marrow-derived endothelial precursor cells restore aging-impaired cardiac angiogenic function. Circ Res 90: E89–E93

    Article  CAS  PubMed  Google Scholar 

  54. Rauscher FM et al. (2003) Aging, progenitor cell exhaustion, and atherosclerosis. Circulation 108: 457–463

    Article  PubMed  Google Scholar 

  55. Wassmann S et al. (2006) Improvement of endothelial function by systemic transfusion of vascular progenitor cells. Circ Res 99: e74–e83

    Article  CAS  PubMed  Google Scholar 

  56. Werner N et al. (2005) Circulating endothelial progenitor cells and cardiovascular outcomes. N Engl J Med 353: 999–1007

    Article  CAS  PubMed  Google Scholar 

  57. Samani NJ et al. (2001) Telomere shortening in atherosclerosis. Lancet 358: 472–473

    Article  CAS  PubMed  Google Scholar 

  58. Satoh M et al. (2008) Association between oxidative DNA damage and telomere shortening in circulating endothelial progenitor cells obtained from metabolic syndrome patients with coronary artery disease. Atherosclerosis [10.1016/j.atherosclerosis.2007.09.040]

  59. Rosso A et al. (2006) p53 Mediates the accelerated onset of senescence of endothelial progenitor cells in diabetes. J Biol Chem 281: 4339–4347

    Article  CAS  PubMed  Google Scholar 

  60. Shantsila, E et al. (2007) Endothelial progenitor cells in cardiovascular disorders. J Am Coll Cardiol 49: 741–752

    Article  CAS  Google Scholar 

  61. Zhu JH et al. (2006) Homocysteine accelerates senescence and reduces proliferation of endothelial progenitor cells. J Mol Cell Cardiol 40: 648–652

    Article  CAS  PubMed  Google Scholar 

  62. Murasawa S et al. (2002) Constitutive human telomerase reverse transcriptase expression enhances regenerative properties of endothelial progenitor cells. Circulation 106: 1133–1139

    Article  CAS  PubMed  Google Scholar 

  63. Spyridopoulos I et al. (2004) Statins enhance migratory capacity by upregulation of the telomere repeat-binding factor TRF2 in endothelial progenitor cells. Circulation 110: 3136–3142

    Article  CAS  PubMed  Google Scholar 

  64. Assmus B et al. (2003) HMG-CoA reductase inhibitors reduce senescence and increase proliferation of endothelial progenitor cells via regulation of cell cycle regulatory genes. Circ Res 92: 1049–1055

    Article  CAS  PubMed  Google Scholar 

  65. Bosch-Marce M et al. (2007) Effects of aging and hypoxia-inducible factor-1 activity on angiogenic cell mobilization and recovery of perfusion after limb ischemia. Circ Res 101: 1310–1318

    Article  CAS  PubMed  Google Scholar 

  66. Chang EI et al. (2007) Age decreases endothelial progenitor cell recruitment through decreases in hypoxia-inducible factor 1alpha stabilization during ischemia. Circulation 116: 2818–2829

    Article  CAS  PubMed  Google Scholar 

  67. Martin GM (2005) Genetic modulation of senescent phenotypes in Homo sapiens. Cell 120: 523–532

    Article  CAS  PubMed  Google Scholar 

  68. Capell B C et al. (2007) Mechanisms of cardiovascular disease in accelerated aging syndromes. Circ Res 101: 13–26

    Article  PubMed  CAS  Google Scholar 

  69. Hennekam RC (2006) Hutchinson–Gilford progeria syndrome: review of the phenotype. Am J Med Genet A 140: 2603–2624

    Article  PubMed  CAS  Google Scholar 

  70. Stehbens WE et al. (1999) Histological and ultrastructural features of atherosclerosis in progeria. Cardiovasc Pathol 8: 29–39

    Article  CAS  PubMed  Google Scholar 

  71. De Sandre-Giovannoli A et al. (2003) Lamin A truncation in Hutchinson–Gilford progeria. Science 300: 2055

    Article  CAS  PubMed  Google Scholar 

  72. Eriksson M et al. (2003) Recurrent de novo point mutations in lamin A cause Hutchinson–Gilford progeria syndrome. Nature 423: 293–298

    Article  CAS  PubMed  Google Scholar 

  73. Mounkes LC et al. (2003) A progeroid syndrome in mice is caused by defects in A-type lamins. Nature 423: 298–301

    Article  CAS  PubMed  Google Scholar 

  74. Varga R et al. (2006) Progressive vascular smooth muscle cell defects in a mouse model of Hutchinson–Gilford progeria syndrome. Proc Natl Acad Sci USA 103: 3250–3255

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  75. Bergo MO et al. (2002) Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defect. Proc Natl Acad Sci USA 99: 13049–13054

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  76. Fong LG et al. (2004) Heterozygosity for Lamin A deficiency eliminates the progeria-like phenotypes in Zmpste24-deficient mice. Proc Natl Acad Sci USA 101: 18111–18116

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  77. Yang SH et al. (2005) Blocking protein farnesyltransferase improves nuclear blebbing in mouse fibroblasts with a targeted Hutchinson–Gilford progeria syndrome mutation. Proc Natl Acad Sci USA 102: 10291–10296

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  78. Varela I et al. (2008) Combined treatment with statins and aminobisphosphonates extends longevity in a mouse model of human premature aging. Nat Med 14: 767–772

    Article  CAS  PubMed  Google Scholar 

  79. Shumaker DK et al. (2006) Mutant nuclear lamin A leads to progressive alterations of epigenetic control in premature aging. Proc Natl Acad Sci USA 103: 8703–8708

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  80. Goldman RD et al. (2004) Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson–Gilford progeria syndrome. Proc Natl Acad Sci USA 101: 8963–8968

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  81. Liu B et al. (2005) Genomic instability in laminopathy-based premature aging. Nat Med 11: 780–785

    Article  CAS  PubMed  Google Scholar 

  82. Varela I et al. (2005) Accelerated ageing in mice deficient in Zmpste24 protease is linked to p53 signalling activation. Nature 437: 564–568

    Article  CAS  PubMed  Google Scholar 

  83. Scaffidi P and Misteli T (2008) Lamin A-dependent misregulation of adult stem cells associated with accelerated ageing. Nat Cell Biol 10: 452–459

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  84. Halaschek-Wiener J and Brooks-Wilson A (2007) Progeria of stem cells: stem cell exhaustion in Hutchinson–Gilford progeria syndrome. J Gerontol A Biol Sci Med Sci 62: 3–8

    Article  PubMed  Google Scholar 

  85. Cohen JI et al. (1987) Cardiovascular features of the Werner syndrome. Am J Cardiol 59: 493–495

    Article  CAS  PubMed  Google Scholar 

  86. Yu CE et al. (1996) Positional cloning of the Werner's syndrome gene. Science 272: 258–262

    Article  CAS  PubMed  Google Scholar 

  87. Opresko PL et al. (2004) Junction of RecQ helicase biochemistry and human disease. J Biol Chem 279: 18099–18102

    Article  CAS  PubMed  Google Scholar 

  88. Lombard DB et al. (2000) Mutations in the WRN gene in mice accelerate mortality in a p53-null background. Mol Cell Biol 20: 3286–3291

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  89. Wang L et al. (2000) Cellular Werner phenotypes in mice expressing a putative dominant-negative human WRN gene. Genetics 154: 357–362

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  90. Lebel M and Leder P (1998) A deletion within the murine Werner syndrome helicase induces sensitivity to inhibitors of topoisomerase and loss of cellular proliferative capacity. Proc Natl Acad Sci USA 95: 13097–13102

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  91. Chang S et al. (2004) Essential role of limiting telomeres in the pathogenesis of Werner syndrome. Nat Genet 36: 877–882

    Article  CAS  PubMed  Google Scholar 

  92. Du X et al. (2004) Telomere shortening exposes functions for the mouse Werner and Bloom syndrome genes. Mol Cell Biol 24: 8437–8446

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  93. Wyllie FS et al. (2000) Telomerase prevents the accelerated cell ageing of Werner syndrome fibroblasts. Nat Genet 24: 16–17

    Article  CAS  PubMed  Google Scholar 

  94. Crabbe L et al. (2007) Telomere dysfunction as a cause of genomic instability in Werner syndrome. Proc Natl Acad Sci USA 104: 2205–2210

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  95. Massip L et al. (2006) Increased insulin, triglycerides, reactive oxygen species, and cardiac fibrosis in mice with a mutation in the helicase domain of the Werner syndrome gene homologue. Exp Gerontol 41: 157–168

    Article  CAS  PubMed  Google Scholar 

  96. Ogawa D et al. (2006) Activation of peroxisome proliferator-activated receptor gamma suppresses telomerase activity in vascular smooth muscle cells. Circ Res 98: e50–e59

    Article  CAS  PubMed  Google Scholar 

  97. Bode-Boger SM et al. (2005) Aspirin reduces endothelial cell senescence. Biochem Biophys Res Commun 334: 1226–1232

    Article  PubMed  CAS  Google Scholar 

  98. Komarov PG et al. (1999) A chemical inhibitor of p53 that protects mice from the side effects of cancer therapy. Science 285: 1733–1737

    Article  CAS  PubMed  Google Scholar 

  99. Russell SJ and Kahn CR (2007) Endocrine regulation of ageing. Nat Rev Mol Cell Biol 8: 681–691

    Article  CAS  PubMed  Google Scholar 

  100. Krishnamurthy J et al. (2004) Ink4a/Arf expression is a biomarker of aging. J Clin Invest 114: 1299–1307

    Article  CAS  PubMed  PubMed Central  Google Scholar 

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Acknowledgements

T Minamino was supported by a Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan and by grants from the Suzuken Memorial Foundation, the Japan Diabetes Foundation, the Ichiro Kanehara Foundation, the Tokyo Biochemical Research Foundation, and the Takeda Science Foundation. I Komuro was supported by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science, Sports, and Culture and by Health and Labor Sciences Research grants.

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  1. T Minamino is Assistant Professor at the Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine, and a Research Scientist at Japan Science and Technology Agency, Saitama, Japan.,

    Tohru Minamino

  2. I Komuro is Professor and Chairman of the Department of Cardiovascular Science and Medicine at Chiba University Graduate School of Medicine and Director of the Center for Cardiovascular Interventions at Chiba University Hospital, Chiba, Japan.,

    Issei Komuro

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Correspondence to Issei Komuro.

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Minamino, T., Komuro, I. Vascular aging: insights from studies on cellular senescence, stem cell aging, and progeroid syndromes. Nat Rev Cardiol 5, 637–648 (2008). https://doi.org/10.1038/ncpcardio1324

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