Advances in the ADAMTS Family in Cardiovascular Disease
Keywords:
ADAMTSs, Dilated Cardiomyopathy, Acute Coronary Syndrome, Atherosclerosis
Abstract
Cardiovascular disease is a serious threat to human life and health. The number of people who die from cardiovascular disease is up to 15 million every year, ranking the first cause of all causes of death. ADAMTS family (A Disintegrin and Metalloproteinase With Thrombospondin Motifs, ADAMTSs) are matrix-associated zinc metallopeptidases with secretory function. It has diverse roles in tissue morphogenesis, pathophysiological remodeling, inflammation, and vascular biology. Controlling the structure and function of the Extracellular Matrix (ECM) is the central theme of the biology of ADAMTSs. ADAMTSs mainly play a biological role by regulating the structure and function of extracellular mechanisms, and the abnormal expression or dysfunction of some family members is associated with cardiovascular diseases. ADAMTS family plays an important role in the occurrence and development of various cardiovascular diseases. This paper aims to study the role of ADAMTS family in cardiovascular diseases.
References
[1] Chinese Journal of Cardiovascular Health and Disease Report 2020[J]. Journal of Cardiovascular Disease,2021,40(10):1005-1009.
[2] Porter S, Clark I M, Kevorkian L, et al. The ADAMTS metalloproteinases[J]. Biochemical Journal, 2005, 386(1): 15-27.
[3] RodrÃguez-Manzaneque J C, Fernández-RodrÃguez R, RodrÃguez-Baena F J, et al. ADAMTS proteases in vascular biology[J]. Matrix Biology, 2015, 44: 38-45.
[4] Zhong S, Khalil R A. A Disintegrin and Metalloproteinase (ADAM) and ADAM with thrombospondin motifs (ADAMTS) family in vascular biology and disease[J]. Biochemical pharmacology, 2019, 164: 188-204.
[5] Shiomi T, Lemaître V, D'Armiento J, et al. Matrix metalloproteinases, a disintegrin and metalloproteinases, and a disintegrin and metalloproteinases with thrombospondin motifs in nonâ€neoplastic diseases[J]. Pathology international, 2010, 60(7): 477-496.
[6] Chinese Cardiovascular health and disease Report Compilation Committee. China Cardiovascular health and disease report 2021: latest summary. Biomedical Environmental Sciences, 2012,7; 35 (7) :573-603.
[7] Xie Y, Li M, Wang X, et al. In vivo delivery of adenoviral vector containing interleukin-17 receptor a reduces cardiac remodeling and improves myocardial function in viral myocarditis leading to dilated cardiomyopathy[J]. PLoS One, 2013, 8(8): e72158.
[8] Huang Y, Xia J, Zheng J, et al. Deficiency of cartilage oligomeric matrix protein causes dilated cardiomyopathy[J]. Basic research in cardiology, 2013, 108: 1-21.
[9] Rau C D, Romay M C, Tuteryan M, et al. Systems genetics approach identifies gene pathways and Adamts2 as drivers of isoproterenol-induced cardiac hypertrophy and cardiomyopathy in mice[J]. Cell systems, 2017, 4(1): 121-128. e4.
[10] Wang X, Chen W, Zhang J, et al. Critical role of ADAMTS2 (a disintegrin and metalloproteinase with thrombospondin motifs 2) in cardiac hypertrophy induced by pressure overload[J]. Hypertension, 2017, 69(6): 1060-1069.
[11] Omura J, Satoh K, Kikuchi N, et al. ADAMTS8 promotes the development of pulmonary arterial hypertension and right ventricular failure: a possible novel therapeutic target[J]. Circulation research, 2019, 125(10): 884-906.
[12] Pelisek J, Deutsch L, Ansel A, et al. Expression of a metalloproteinase family of ADAMTS in human vulnerable carotid lesions[J]. Journal of cardiovascular medicine, 2017, 18(1): 10-18.
[13] Jönsson-Rylander A C, Nilsson T, Fritsche-Danielson R, et al. Role of ADAMTS-1 in atherosclerosis: remodeling of carotid artery, immunohistochemistry, and proteolysis of versican[J]. Arteriosclerosis, thrombosis, and vascular biology, 2005, 25(1): 180-185.
[14] Pehlivan S, Gurses M S, Ural M N, et al. The role of ADAMTS1 and versican in human myocardial infarction: a postmortem study[J]. Laboratory Medicine, 2016, 47(3): 205-212.
[15] Lee C W, Hwang I, Park C S, et al. Expression of ADAMTS-2,-3,-13, and-14 in culprit coronary lesions in patients with acute myocardial infarction or stable angina[J]. Journal of thrombosis and thrombolysis, 2012, 33: 362-370.
[16] Ren P, Zhang L, Xu G, et al. ADAMTS-1 and ADAMTS-4 levels are elevated in thoracic aortic aneurysms and dissections[J]. The Annals of thoracic surgery, 2013, 95(2): 570-577.
[17] Chen L, Yang L, Zha Y, et al. Association of serum a disintegrin and metalloproteinase with thrombospodin motif 4 levels with the presence and severity of coronary artery disease[J]. Coronary artery disease, 2011, 22(8): 570-576.
[18] Uluçay S, Çam F S, Batır M B, et al. A novel association between TGFβl and ADAMTS4 in coronary artery disease: A new potential mechanism in the progression of atherosclerosis and diabetes[J]. Anatolian journal of cardiology, 2015, 15(10): 823.
[19] Zha Y, Chen Y, Xu F, et al. ADAMTS4 level in patients with stable coronary artery disease and acute coronary syndromes[J]. Biomedicine & pharmacotherapy, 2010, 64(3): 160-164.
[20] Wågsäter D, Björk H, Zhu C, et al. ADAMTS-4 and-8 are inflammatory regulated enzymes expressed in macrophage-rich areas of human atherosclerotic plaques[J]. Atherosclerosis, 2008, 196(2): 514-522.
[21] Zha Y, Chen Y, Xu F, et al. Elevated level of ADAMTS4 in plasma and peripheral monocytes from patients with acute coronary syndrome[J]. Clinical Research in Cardiology, 2010, 99: 781-786.
[22] Dong H, Du T, Premaratne S, et al. Relationship between ADAMTS4 and carotid atherosclerotic plaque vulnerability in humans[J]. Journal of Vascular Surgery, 2018, 67(4): 1120-1126.
[23] Chen Y C, Bui A V, Diesch J, et al. A novel mouse model of atherosclerotic plaque instability for drug testing and mechanistic/therapeutic discoveries using gene and microRNA expression profiling[J]. Circulation research, 2013, 113(3): 252-265.
[24] Bauer R C, Tohyama J, Cui J, et al. Knockout of Adamts7, a novel coronary artery disease locus in humans, reduces atherosclerosis in mice[J]. Circulation, 2015, 131(13): 1202-1213.
[25] Pu X, Xiao Q, Kiechl S, et al. ADAMTS7 cleavage and vascular smooth muscle cell migration are affected by a coronary-artery-disease-associated variant[J]. The American Journal of Human Genetics, 2013, 92(3): 366-374.
[26] Bengtsson E, Hultman K, Dunér P, et al. ADAMTS-7 is associated with a high-risk plaque phenotype in human atherosclerosis[J]. Scientific reports, 2017, 7(1): 3753.
[27] Yu J, Zhou B, Yu H, et al. Association between plasma ADAMTS-7 levels and severity of disease in patients with stable obstructive coronary artery disease[J]. Medicine, 2016, 95(48).
[28] Kessler T, Zhang L, Liu Z, et al. ADAMTS-7 inhibits re-endothelialization of injured arteries and promotes vascular remodeling through cleavage of thrombospondin-1[J]. Circulation, 2015, 131(13): 1191-1201.
[29] Wang L, Zheng J, Bai X, et al. ADAMTS-7 mediates vascular smooth muscle cell migration and neointima formation in balloon-injured rat arteries[J]. Circulation research, 2009, 104(5): 688-698.
[30] Riessen R, Fenchel M, Chen H, et al. Cartilage oligomeric matrix protein (thrombospondin-5) is expressed by human vascular smooth muscle cells[J]. Arteriosclerosis, thrombosis, and vascular biology, 2001, 21(1): 47-54.
[31] Wang L, Wang X, Kong W. ADAMTS-7, a novel proteolytic culprit in vascular remodeling[J]. Sheng li xue bao:[Acta Physiologica Sinica], 2010, 62(4): 285-294.
[32] Wang L, Zheng J, Bai X, et al. ADAMTS-7 mediates vascular smooth muscle cell migration and neointima formation in balloon-injured rat arteries[J]. Circulation research, 2009, 104(5): 688-698.
[33] Reilly M P, Li M, He J, et al. Identification of ADAMTS7 as a novel locus for coronary atherosclerosis and association of ABO with myocardial infarction in the presence of coronary atherosclerosis: two genome-wide association studies[J]. The Lancet, 2011, 377(9763): 383-392.
[34] Du Y, Gao C, Liu Z, et al. Upregulation of a disintegrin and metalloproteinase with thrombospondin motifs-7 by miR-29 repression mediates vascular smooth muscle calcification[J]. Arteriosclerosis, thrombosis, and vascular biology, 2012, 32(11): 2580-2588.
[35] Bengtsson E, Hultman K, Dunér P, et al. ADAMTS-7 is associated with a high-risk plaque phenotype in human atherosclerosis[J]. Scientific reports, 2017, 7(1): 3753.
[36] De Meyer S F, Savchenko A S, Haas M S, et al. Protective anti-inflammatory effect of ADAMTS13 on myocardial ischemia/reperfusion injury in mice[J]. Blood, The Journal of the American Society of Hematology, 2012, 120(26): 5217-5223.
[37] Gandhi C, Motto D G, Jensen M, et al. ADAMTS13 deficiency exacerbates VWF-dependent acute myocardial ischemia/reperfusion injury in mice[J]. Blood, The Journal of the American Society of Hematology, 2012, 120(26): 5224-5230.
[38] Doi M, Matsui H, Takeda Y, et al. ADAMTS13 safeguards the myocardium in a mouse model of acute myocardial infarction[J]. Thrombosis and haemostasis, 2012, 108(12): 1236-1238.
[39] Sonneveld M A H, de Maat M P M, Leebeek F W G. Von Willebrand factor and ADAMTS13 in arterial thrombosis: a systematic review and meta-analysis[J]. Blood reviews, 2014, 28(4): 167-178.
[40] Maino A, Siegerink B, Lotta L A, et al. Plasma ADAMTSâ€13 levels and the risk of myocardial infarction: an individual patient data metaâ€analysis[J]. Journal of Thrombosis and Haemostasis, 2015, 13(8): 1396-1404.
[41] Lv C L, Chen C, Zheng Z,Liu P, He X W, Jin X P,et al. Association between ADAMTS-1 gene polymorphism and essential hypertension in Chinese Han population [J]. Zhejiang Med,2018, 40(01):19-22.
[42] Liu C, Wang X, Shang L X,et al. Expression of ADAMTS-2 and ADAMTS-7 in placenta with gestational hypertension [J]. Chinese People's Armed Police Medicine,2013,24(08):695-698.
[43] Cerveró J, Segura V, MacÃas A, et al. Atrial fibrillation in pigs induces left atrial endocardial transcriptional remodelling[J]. Thrombosis and haemostasis, 2012, 108(10): 742-749.
[44] Freynhofer M K, Gruber S C, Bruno V, et al.Prognostic value of plasma von Willebrand factor and its cleaving protease ADAMTS13 in patients wit-h atrial fibrillation[J]. International journal of cardiology, 2013, 168(1): 317-325.
[45] Wang H J, Xiao M, Zeng Z, et al.Correlation analysis between ADAMTS-13 gene polymorphism and hypertension-induced atrial fibrillation[J].Eur Rev Med Pharmacol Sci, 2020, 24(5): 2674.
[46] Dupuis L E, McCulloch D R, McGarity J D, et al. Altered versican cleavage in ADAMTS5 deficient mice; a novel etiology of myxomatous valve disease[J]. Developmental biology, 2011, 357(1): 152-164.
[47] Kern C B, Wessels A, McGarity J, et al. Reduced versican cleavage due to Adamts9 haploinsufficiency is associated with cardiac and aortic anomalies[J]. Matrix biology, 2010, 29(4): 304-316.
[48] Wünnemann F, Ta-Shma A, Preuss C, et al. Loss of ADAMTS19 causes progressive non-syndromic heart valve disease[J]. Nature genetics, 2020, 52(1): 40-47.
[49] Massadeh S, Alhashem A, van de Laar I M B H, et al. ADAMTS19â€associated heart valve defects: Novel genetic variants consolidating a recognizable cardiac phenotype[J]. Clinical Genetics, 2020, 98(1): 56-63.
[2] Porter S, Clark I M, Kevorkian L, et al. The ADAMTS metalloproteinases[J]. Biochemical Journal, 2005, 386(1): 15-27.
[3] RodrÃguez-Manzaneque J C, Fernández-RodrÃguez R, RodrÃguez-Baena F J, et al. ADAMTS proteases in vascular biology[J]. Matrix Biology, 2015, 44: 38-45.
[4] Zhong S, Khalil R A. A Disintegrin and Metalloproteinase (ADAM) and ADAM with thrombospondin motifs (ADAMTS) family in vascular biology and disease[J]. Biochemical pharmacology, 2019, 164: 188-204.
[5] Shiomi T, Lemaître V, D'Armiento J, et al. Matrix metalloproteinases, a disintegrin and metalloproteinases, and a disintegrin and metalloproteinases with thrombospondin motifs in nonâ€neoplastic diseases[J]. Pathology international, 2010, 60(7): 477-496.
[6] Chinese Cardiovascular health and disease Report Compilation Committee. China Cardiovascular health and disease report 2021: latest summary. Biomedical Environmental Sciences, 2012,7; 35 (7) :573-603.
[7] Xie Y, Li M, Wang X, et al. In vivo delivery of adenoviral vector containing interleukin-17 receptor a reduces cardiac remodeling and improves myocardial function in viral myocarditis leading to dilated cardiomyopathy[J]. PLoS One, 2013, 8(8): e72158.
[8] Huang Y, Xia J, Zheng J, et al. Deficiency of cartilage oligomeric matrix protein causes dilated cardiomyopathy[J]. Basic research in cardiology, 2013, 108: 1-21.
[9] Rau C D, Romay M C, Tuteryan M, et al. Systems genetics approach identifies gene pathways and Adamts2 as drivers of isoproterenol-induced cardiac hypertrophy and cardiomyopathy in mice[J]. Cell systems, 2017, 4(1): 121-128. e4.
[10] Wang X, Chen W, Zhang J, et al. Critical role of ADAMTS2 (a disintegrin and metalloproteinase with thrombospondin motifs 2) in cardiac hypertrophy induced by pressure overload[J]. Hypertension, 2017, 69(6): 1060-1069.
[11] Omura J, Satoh K, Kikuchi N, et al. ADAMTS8 promotes the development of pulmonary arterial hypertension and right ventricular failure: a possible novel therapeutic target[J]. Circulation research, 2019, 125(10): 884-906.
[12] Pelisek J, Deutsch L, Ansel A, et al. Expression of a metalloproteinase family of ADAMTS in human vulnerable carotid lesions[J]. Journal of cardiovascular medicine, 2017, 18(1): 10-18.
[13] Jönsson-Rylander A C, Nilsson T, Fritsche-Danielson R, et al. Role of ADAMTS-1 in atherosclerosis: remodeling of carotid artery, immunohistochemistry, and proteolysis of versican[J]. Arteriosclerosis, thrombosis, and vascular biology, 2005, 25(1): 180-185.
[14] Pehlivan S, Gurses M S, Ural M N, et al. The role of ADAMTS1 and versican in human myocardial infarction: a postmortem study[J]. Laboratory Medicine, 2016, 47(3): 205-212.
[15] Lee C W, Hwang I, Park C S, et al. Expression of ADAMTS-2,-3,-13, and-14 in culprit coronary lesions in patients with acute myocardial infarction or stable angina[J]. Journal of thrombosis and thrombolysis, 2012, 33: 362-370.
[16] Ren P, Zhang L, Xu G, et al. ADAMTS-1 and ADAMTS-4 levels are elevated in thoracic aortic aneurysms and dissections[J]. The Annals of thoracic surgery, 2013, 95(2): 570-577.
[17] Chen L, Yang L, Zha Y, et al. Association of serum a disintegrin and metalloproteinase with thrombospodin motif 4 levels with the presence and severity of coronary artery disease[J]. Coronary artery disease, 2011, 22(8): 570-576.
[18] Uluçay S, Çam F S, Batır M B, et al. A novel association between TGFβl and ADAMTS4 in coronary artery disease: A new potential mechanism in the progression of atherosclerosis and diabetes[J]. Anatolian journal of cardiology, 2015, 15(10): 823.
[19] Zha Y, Chen Y, Xu F, et al. ADAMTS4 level in patients with stable coronary artery disease and acute coronary syndromes[J]. Biomedicine & pharmacotherapy, 2010, 64(3): 160-164.
[20] Wågsäter D, Björk H, Zhu C, et al. ADAMTS-4 and-8 are inflammatory regulated enzymes expressed in macrophage-rich areas of human atherosclerotic plaques[J]. Atherosclerosis, 2008, 196(2): 514-522.
[21] Zha Y, Chen Y, Xu F, et al. Elevated level of ADAMTS4 in plasma and peripheral monocytes from patients with acute coronary syndrome[J]. Clinical Research in Cardiology, 2010, 99: 781-786.
[22] Dong H, Du T, Premaratne S, et al. Relationship between ADAMTS4 and carotid atherosclerotic plaque vulnerability in humans[J]. Journal of Vascular Surgery, 2018, 67(4): 1120-1126.
[23] Chen Y C, Bui A V, Diesch J, et al. A novel mouse model of atherosclerotic plaque instability for drug testing and mechanistic/therapeutic discoveries using gene and microRNA expression profiling[J]. Circulation research, 2013, 113(3): 252-265.
[24] Bauer R C, Tohyama J, Cui J, et al. Knockout of Adamts7, a novel coronary artery disease locus in humans, reduces atherosclerosis in mice[J]. Circulation, 2015, 131(13): 1202-1213.
[25] Pu X, Xiao Q, Kiechl S, et al. ADAMTS7 cleavage and vascular smooth muscle cell migration are affected by a coronary-artery-disease-associated variant[J]. The American Journal of Human Genetics, 2013, 92(3): 366-374.
[26] Bengtsson E, Hultman K, Dunér P, et al. ADAMTS-7 is associated with a high-risk plaque phenotype in human atherosclerosis[J]. Scientific reports, 2017, 7(1): 3753.
[27] Yu J, Zhou B, Yu H, et al. Association between plasma ADAMTS-7 levels and severity of disease in patients with stable obstructive coronary artery disease[J]. Medicine, 2016, 95(48).
[28] Kessler T, Zhang L, Liu Z, et al. ADAMTS-7 inhibits re-endothelialization of injured arteries and promotes vascular remodeling through cleavage of thrombospondin-1[J]. Circulation, 2015, 131(13): 1191-1201.
[29] Wang L, Zheng J, Bai X, et al. ADAMTS-7 mediates vascular smooth muscle cell migration and neointima formation in balloon-injured rat arteries[J]. Circulation research, 2009, 104(5): 688-698.
[30] Riessen R, Fenchel M, Chen H, et al. Cartilage oligomeric matrix protein (thrombospondin-5) is expressed by human vascular smooth muscle cells[J]. Arteriosclerosis, thrombosis, and vascular biology, 2001, 21(1): 47-54.
[31] Wang L, Wang X, Kong W. ADAMTS-7, a novel proteolytic culprit in vascular remodeling[J]. Sheng li xue bao:[Acta Physiologica Sinica], 2010, 62(4): 285-294.
[32] Wang L, Zheng J, Bai X, et al. ADAMTS-7 mediates vascular smooth muscle cell migration and neointima formation in balloon-injured rat arteries[J]. Circulation research, 2009, 104(5): 688-698.
[33] Reilly M P, Li M, He J, et al. Identification of ADAMTS7 as a novel locus for coronary atherosclerosis and association of ABO with myocardial infarction in the presence of coronary atherosclerosis: two genome-wide association studies[J]. The Lancet, 2011, 377(9763): 383-392.
[34] Du Y, Gao C, Liu Z, et al. Upregulation of a disintegrin and metalloproteinase with thrombospondin motifs-7 by miR-29 repression mediates vascular smooth muscle calcification[J]. Arteriosclerosis, thrombosis, and vascular biology, 2012, 32(11): 2580-2588.
[35] Bengtsson E, Hultman K, Dunér P, et al. ADAMTS-7 is associated with a high-risk plaque phenotype in human atherosclerosis[J]. Scientific reports, 2017, 7(1): 3753.
[36] De Meyer S F, Savchenko A S, Haas M S, et al. Protective anti-inflammatory effect of ADAMTS13 on myocardial ischemia/reperfusion injury in mice[J]. Blood, The Journal of the American Society of Hematology, 2012, 120(26): 5217-5223.
[37] Gandhi C, Motto D G, Jensen M, et al. ADAMTS13 deficiency exacerbates VWF-dependent acute myocardial ischemia/reperfusion injury in mice[J]. Blood, The Journal of the American Society of Hematology, 2012, 120(26): 5224-5230.
[38] Doi M, Matsui H, Takeda Y, et al. ADAMTS13 safeguards the myocardium in a mouse model of acute myocardial infarction[J]. Thrombosis and haemostasis, 2012, 108(12): 1236-1238.
[39] Sonneveld M A H, de Maat M P M, Leebeek F W G. Von Willebrand factor and ADAMTS13 in arterial thrombosis: a systematic review and meta-analysis[J]. Blood reviews, 2014, 28(4): 167-178.
[40] Maino A, Siegerink B, Lotta L A, et al. Plasma ADAMTSâ€13 levels and the risk of myocardial infarction: an individual patient data metaâ€analysis[J]. Journal of Thrombosis and Haemostasis, 2015, 13(8): 1396-1404.
[41] Lv C L, Chen C, Zheng Z,Liu P, He X W, Jin X P,et al. Association between ADAMTS-1 gene polymorphism and essential hypertension in Chinese Han population [J]. Zhejiang Med,2018, 40(01):19-22.
[42] Liu C, Wang X, Shang L X,et al. Expression of ADAMTS-2 and ADAMTS-7 in placenta with gestational hypertension [J]. Chinese People's Armed Police Medicine,2013,24(08):695-698.
[43] Cerveró J, Segura V, MacÃas A, et al. Atrial fibrillation in pigs induces left atrial endocardial transcriptional remodelling[J]. Thrombosis and haemostasis, 2012, 108(10): 742-749.
[44] Freynhofer M K, Gruber S C, Bruno V, et al.Prognostic value of plasma von Willebrand factor and its cleaving protease ADAMTS13 in patients wit-h atrial fibrillation[J]. International journal of cardiology, 2013, 168(1): 317-325.
[45] Wang H J, Xiao M, Zeng Z, et al.Correlation analysis between ADAMTS-13 gene polymorphism and hypertension-induced atrial fibrillation[J].Eur Rev Med Pharmacol Sci, 2020, 24(5): 2674.
[46] Dupuis L E, McCulloch D R, McGarity J D, et al. Altered versican cleavage in ADAMTS5 deficient mice; a novel etiology of myxomatous valve disease[J]. Developmental biology, 2011, 357(1): 152-164.
[47] Kern C B, Wessels A, McGarity J, et al. Reduced versican cleavage due to Adamts9 haploinsufficiency is associated with cardiac and aortic anomalies[J]. Matrix biology, 2010, 29(4): 304-316.
[48] Wünnemann F, Ta-Shma A, Preuss C, et al. Loss of ADAMTS19 causes progressive non-syndromic heart valve disease[J]. Nature genetics, 2020, 52(1): 40-47.
[49] Massadeh S, Alhashem A, van de Laar I M B H, et al. ADAMTS19â€associated heart valve defects: Novel genetic variants consolidating a recognizable cardiac phenotype[J]. Clinical Genetics, 2020, 98(1): 56-63.
Published
2023-06-01
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Copyright (c) 2023 Tianying Jin
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