细胞外基质重建规律衍变与梗死后缺血心肌纤维化发生
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摘要
细胞外基质(extracellular matrix,ECM)是梗死后缺血心肌纤维化发生的主要病理产物,随着病程进展而出现重建规律的衍变:炎症期坏死胶原基质瓦解,临时基质网络形成;增殖期基质细胞蛋白富集,肌成纤维细胞活化;修复期胶原基质瘢痕稳定,基质蛋白时序清除。靶向干预ECM降解、优化调节ECM分泌能够为心脏再生提供骨架支撑、维持心脏结构完整和舒缩韧性的同时,防止异常ECM重建带来的心脏功能衰竭。
Extracellular matrix( ECM) is the main pathological product during fibrogenesis in ischemic myocardium after myocardial infarction. The progression and reconstruction rules of ECM develop along with different periods of the disease: in the inflammatory stage. A temporary matrix network forms with the degradation of original collagen matrix. In the proliferative stage,the enrichment of matricellular proteins activates myofibroblasts In the reparative stage,a stable collagen matrix network is established and temporary matrix proteins are removed punctually. Targeting the degradation of ECM and optimizing the secretion of ECM proteins will provide a complete skeleton support for cardiac regeneration,maintain the integrated heart structure and diastolic toughness,and then prevent heart function failure owing to abnormal ECM reconstruction.
Extracellular matrix( ECM) is the main pathological product during fibrogenesis in ischemic myocardium after myocardial infarction. The progression and reconstruction rules of ECM develop along with different periods of the disease: in the inflammatory stage. A temporary matrix network forms with the degradation of original collagen matrix. In the proliferative stage,the enrichment of matricellular proteins activates myofibroblasts In the reparative stage,a stable collagen matrix network is established and temporary matrix proteins are removed punctually. Targeting the degradation of ECM and optimizing the secretion of ECM proteins will provide a complete skeleton support for cardiac regeneration,maintain the integrated heart structure and diastolic toughness,and then prevent heart function failure owing to abnormal ECM reconstruction.
引文
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[10]Wells JM,Gaggar A,Blalock JE. MMP generated matrikines[J].Matrix Biol,2015,44-46:122-129.
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[15]Bellon G,Martiny L,Robinet A. Matrix metalloproteinases andmatrikines in angiogenesis[J]. Crit Rev Oncol Hematol,2004,49(3):203-220.
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[17]Gaggar A,Jackson PL,Noerager BD,et al. A novel proteolytic cas-cade generates an extracellular matrix-derived chemoattractant inchronic neutrophilic inflammation[J]. J Immunol,2008,180(8):5662-5669.
[18]Lindsey ML,Iyer RP,Zamilpa R,et al. A novel collagen matric-ryptin reduces left ventricular dilation post-myocardial infarction bypromoting scar formation and angiogenesis[J]. J Am Coll Cardiol,2015,66(12):1364-1374.
[19]Okada M,Oba Y,Yamawaki H. Endostatin stimulates proliferationand migration of adult rat cardiac fibroblasts through PI3K/Akt path-way[J]. Eur J Pharmacol,2015,750:20-26.
[20]Heljasvaara R,Nyberg P,Luostarinen J,et al. Generation of biolog-ically active endostatin fragments from human collagen XVIII bydistinct matrix metalloproteases[J]. Exp Cell Res,2005,307(2):292-304.
[21]Arslan F,Smeets MB,Vis P WR,et al. Lack of Fibronectin-EDApromotes survival and prevents adverse remodeling and heart functiondeterioration after myocardial infarction[J]. Circ Res,2011,108(5):582-592.
[22]Andersson L,Scharin TM,Lundqvist A,et al. Rip2 modifiesVEGF-induced signalling and vascular permeability in myocardialischaemia[J]. Cardiovasc Res,2015,107(4):478-486.
[23]Martino MM,Briquez PS,Ranga A,et al. Heparin-binding domainof fibrin(ogen)binds growth factors and promotes tissue repair whenincorporated within a synthetic matrix[J]. Proc Natl Acad Sci U SA,2013,110(12):4563-4568.
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[25]Motley MP,Madsen DH,Jürgensen HJ,et al. ACCR2 macrophageendocytic pathway mediates extravascular fibrin clearance in vivo[J]. Blood,2015,127(9):1085-1096.
[26]Chistiakov DA,Melnichenko AA,Myasoedova VA,et al. Throm-bospondins:a role in cardiovascular disease[J]. Int J Mol Sci,2017,18(7):1540.
[27]Bhattacharyya S,Wang W,Moralesnebreda L,et al. Tenascin-Cdrives persistence of organ fibrosis[J]. Nat Commun,2016,7:11703.
[28]Zhao H,Wang W,Zhang J,et al. Inhibition of osteopontin reducethe cardiac myofibrosis in dilated cardiomyopathy via focal adhesionkinase mediated signaling pathway[J]. Am J Transl Res,2016,8(9):3645-3655.
[29]Zhao S,Wu H,Xia W. Periostin expression is upregulated andassociated with myocardial fibrosis in human failing hearts[J].J Cardiol,2014,63(5):373-378.
[30]Díez J,González A,Ravassa S. Understanding the role of CCNmatricellular proteins in myocardial fibrosis[J]. J Am Coll Cardiol,2016,67(13):1569-1571.
[31]Li L,Zhao Q,Kong W. Extracellular matrix remodeling and cardiacfibrosis[J]. Matrix Biol,2018,68-69:409-506.
[32]Van der Smissen A,Hintze V,et al. Artificial extracellular matrixcomposed of collagen I and highly sulfated hyaluronan interferes withTGF-β1 signaling and prevents TGF-β1 induced myofibroblast differ-entiation[J]. Acta Biomater,2013,9(8):7775-7786.
[33]Huebener P,Abou-Khamis T,Zymek P,et al. CD44 is criticallyinvolved in infarct healing by regulating the inflammatory and fibroticresponse[J]. J Immunol,2008,180(4):2625-2633.
[34]Hattori N,Carrino DA,Lauer ME,et al. Pericellular versican regu-lates the fibroblast myofibroblast transition:A role for ADAMTS5protease mediated proteolysis[J]. J Biol Chem,2011,286(39):34298-34310.
[35]Keane TJ,Horejs CM,Stevens MM. Scarring vs. functional heal-ing:Matrix-based strategies to regulate tissue repair[J]. Adv DrugDeliv Rev,2018,129:407-419.
[36]Van De WL,Varney S,Tomasek JJ. Mechanoregulation of the myofi-broblast in wound contraction,scarring,and fibrosis:opportunities fornew therapeutic intervention[J]. Adv Wound Care(New Rochelle),2013,2(4):122-141.
[37]Rienks M,Papageorgiou AP,Frangogiannis NG,et al. Myocardialextracellular matrix:an ever-changing and diverse entity[J]. CircRes,2014,114(5):872-888.
[38]Hudson MP,Armstrong PW,Ruzyllo W,et al. Effects of selectivematrix metalloproteinase inhibitor(PG-116800)to prevent ventricularremodeling after myocardial infarction:results of the PREMIER(Pre-vention of Myocardial Infarction Early Remodeling)trial[J]. J AmColl Cardiol,2006,48(1):15-20.
[39]Cerisano G,Buonamici P,Valenti R,et al. Early short-term doxy-cycline therapy in patients with acute myocardial infarction and leftventricular dysfunction and the ominous progression to adverse remod-eling(TIPTOP). A randomized controlled trial[J]. J Am Coll Cardi-ol,2012,59(13):E349.
[40] Okamoto H, Imanaka-Yoshida K. Matricellular proteins:newmolecular targets to prevent heart failure[J]. Cardiovasc Ther,2012,30(4):e198-e209.
[41]Behfar A,Crespo-Diaz R,Terzic A,et al. Cell therapy for cardiacrepair-lessons from clinical trials[J]. Nat Rev Cardiol,2014,11(4):232-246.
[42]Qiu Y,Bayomy AF,Gomez MV,et al. A role for matrix stiffness inthe regulation of cardiac side population cell function[J]. Am J Phys-iol Heart Circ Physiol,2015,308(9):H990-H997.
[43]Chen WC,Wang Z,Missinato MA,et al. Decellularized zebrafishcardiac extracellular matrix induces mammalian heart regeneration[J]. Sci Adv,2016,2(11):e1600844.
[44]Wang J,Karra R,Dickson AL,et al. Fibronectin is deposited by in-jury-activated epicardial cells and is necessary for zebrafish heart re-generation[J]. Dev Biol,2013,382(2):427-435.
[45]Patterson NL,Iyer RP,de Castro Brás LE,et al. Using proteomics touncover extracellular matrix interactions during cardiac remodeling[J]. Proteomics Clin Appl,2013,7(7-8):516-527.
[46]Barallobrebarreiro J,Didangelos A,Schoendube FA,et al. Pro-teomics analysis of cardiac extracellular matrix remodeling in a porcinemodel of ischemia/reperfusion injury clinical perspective[J]. Circula-tion,2012,125(6):789-802.
[47]Deaguero JL,Mckown EN,Zhang L,et al. Altered protein levels inthe isolated extracellular matrix of failing human hearts with dilatedcardiomyopathy[J]. Cardiovasc Pathol,2017,26:12-20.
[48]Spinale FG,Zile MR. Integrating the myocardial matrix into heartfailure recognition and management[J]. Circ Res,2013,113(6):725-738.
[49]Lindsey ML,Hall ME,Harmancey R,et al. Adapting extracellularmatrix proteomics for clinical studies on cardiac remodeling post-myo-cardial infarction[J]. Clin Proteomics,2016,13(1):19.
[2]Gulati A,Jabbour A,Ismail TF,et al. Association of fibrosis withmortality and sudden cardiac death in patients with nonischemicdilated cardiomyopathy[J]. JAMA,2013,309(9):896-908.
[3] Frangogiannis NG. Matricellular proteins in cardiac adaptation anddisease[J]. Physiol Rev,2012,92(2):635-688.
[4] Prabhu SD,Frangogiannis NG. The biological basis for cardiacrepair after myocardial infarction:from inflammation to fibrosis[J].Circ Res,2016,119(1):91-112.
[5] Ozbek S,Balasubramanian PG,Chiquet-Ehrismann R,et al. Theevolution of extracellular matrix[J]. Mol Biol Cell,2010,21(24):4300-4305.
[6] Frangogiannis NG. Pathophysiology of myocardial infarction[J].Compr Physiol,2015,5(4):1841-1875.
[7]Dobaczewski M,Gonzalezquesada C,Frangogiannis NG. The extra-cellular matrix as a modulator of the inflammatory and reparativeresponse following myocardial infarction[J]. J Mol Cell Cardiol,2010,48(3):504-511.
[8] Wang RM,Christman KL. Decellularized myocardial matrix hydro-gels:in basic research and preclinical studies[J]. Adv Drug DelivRev,2015,96:77-82.
[9]Cauwe B,Opdenakker G. Intracellular substrate cleavage:a noveldimension in the biochemistry,biology and pathology of matrix met-alloproteinases[J]. Crit Rev Biochem Mol Biol,2010,45(5):351-423.
[10]Wells JM,Gaggar A,Blalock JE. MMP generated matrikines[J].Matrix Biol,2015,44-46:122-129.
[11]Jobin PG,Butler GS,Overall C M. New intracellular activities ofmatrix metalloproteinases shine in the moonlight[J]. Biochim Bio-phys Acta Mol Cell Res,2017,1864(11 Pt A):2043-2055.
[12]Ali MA,Cho WJ,Hudson B,et al. Titin is a target of matrix metal-loproteinase-2:implications in myocardial ischemia/reperfusion injury[J]. Circulation,2010,122(20):2039-2047.
[13]Francisco V,Jeffrey O,Wolfgang D,et al. Early degradation andserum appearance of type I collagen fragments after myocardial in-farction[J]. J Mol Cell Cardiol,2004,36(4):597-601.
[14]Lauten A,Gerhard-Garcia A,Suhr F,et al. Impact of ischemia-reperfusion on extracellular matrix processing and structure of thebasement membrane of the heart[J]. PLoS ONE,2014,9(3):e92633.
[15]Bellon G,Martiny L,Robinet A. Matrix metalloproteinases andmatrikines in angiogenesis[J]. Crit Rev Oncol Hematol,2004,49(3):203-220.
[16]Weathington NM,van Houwelingen AH,Noerager BD,et al. Anovel peptide CXCR ligand derived from extracellular matrix degra-dation during airway inflammation[J]. Nat Med,2006,12(3):317-323.
[17]Gaggar A,Jackson PL,Noerager BD,et al. A novel proteolytic cas-cade generates an extracellular matrix-derived chemoattractant inchronic neutrophilic inflammation[J]. J Immunol,2008,180(8):5662-5669.
[18]Lindsey ML,Iyer RP,Zamilpa R,et al. A novel collagen matric-ryptin reduces left ventricular dilation post-myocardial infarction bypromoting scar formation and angiogenesis[J]. J Am Coll Cardiol,2015,66(12):1364-1374.
[19]Okada M,Oba Y,Yamawaki H. Endostatin stimulates proliferationand migration of adult rat cardiac fibroblasts through PI3K/Akt path-way[J]. Eur J Pharmacol,2015,750:20-26.
[20]Heljasvaara R,Nyberg P,Luostarinen J,et al. Generation of biolog-ically active endostatin fragments from human collagen XVIII bydistinct matrix metalloproteases[J]. Exp Cell Res,2005,307(2):292-304.
[21]Arslan F,Smeets MB,Vis P WR,et al. Lack of Fibronectin-EDApromotes survival and prevents adverse remodeling and heart functiondeterioration after myocardial infarction[J]. Circ Res,2011,108(5):582-592.
[22]Andersson L,Scharin TM,Lundqvist A,et al. Rip2 modifiesVEGF-induced signalling and vascular permeability in myocardialischaemia[J]. Cardiovasc Res,2015,107(4):478-486.
[23]Martino MM,Briquez PS,Ranga A,et al. Heparin-binding domainof fibrin(ogen)binds growth factors and promotes tissue repair whenincorporated within a synthetic matrix[J]. Proc Natl Acad Sci U SA,2013,110(12):4563-4568.
[24]Ahrens I,Peter K. FX-06,a fibrin-derived Bbeta15-42 peptidefor the potential treatment of reperfusion injury following myocardialinfarction[J]. Curr Opin Investig Drugs,2009,10(9):997-1003.
[25]Motley MP,Madsen DH,Jürgensen HJ,et al. ACCR2 macrophageendocytic pathway mediates extravascular fibrin clearance in vivo[J]. Blood,2015,127(9):1085-1096.
[26]Chistiakov DA,Melnichenko AA,Myasoedova VA,et al. Throm-bospondins:a role in cardiovascular disease[J]. Int J Mol Sci,2017,18(7):1540.
[27]Bhattacharyya S,Wang W,Moralesnebreda L,et al. Tenascin-Cdrives persistence of organ fibrosis[J]. Nat Commun,2016,7:11703.
[28]Zhao H,Wang W,Zhang J,et al. Inhibition of osteopontin reducethe cardiac myofibrosis in dilated cardiomyopathy via focal adhesionkinase mediated signaling pathway[J]. Am J Transl Res,2016,8(9):3645-3655.
[29]Zhao S,Wu H,Xia W. Periostin expression is upregulated andassociated with myocardial fibrosis in human failing hearts[J].J Cardiol,2014,63(5):373-378.
[30]Díez J,González A,Ravassa S. Understanding the role of CCNmatricellular proteins in myocardial fibrosis[J]. J Am Coll Cardiol,2016,67(13):1569-1571.
[31]Li L,Zhao Q,Kong W. Extracellular matrix remodeling and cardiacfibrosis[J]. Matrix Biol,2018,68-69:409-506.
[32]Van der Smissen A,Hintze V,et al. Artificial extracellular matrixcomposed of collagen I and highly sulfated hyaluronan interferes withTGF-β1 signaling and prevents TGF-β1 induced myofibroblast differ-entiation[J]. Acta Biomater,2013,9(8):7775-7786.
[33]Huebener P,Abou-Khamis T,Zymek P,et al. CD44 is criticallyinvolved in infarct healing by regulating the inflammatory and fibroticresponse[J]. J Immunol,2008,180(4):2625-2633.
[34]Hattori N,Carrino DA,Lauer ME,et al. Pericellular versican regu-lates the fibroblast myofibroblast transition:A role for ADAMTS5protease mediated proteolysis[J]. J Biol Chem,2011,286(39):34298-34310.
[35]Keane TJ,Horejs CM,Stevens MM. Scarring vs. functional heal-ing:Matrix-based strategies to regulate tissue repair[J]. Adv DrugDeliv Rev,2018,129:407-419.
[36]Van De WL,Varney S,Tomasek JJ. Mechanoregulation of the myofi-broblast in wound contraction,scarring,and fibrosis:opportunities fornew therapeutic intervention[J]. Adv Wound Care(New Rochelle),2013,2(4):122-141.
[37]Rienks M,Papageorgiou AP,Frangogiannis NG,et al. Myocardialextracellular matrix:an ever-changing and diverse entity[J]. CircRes,2014,114(5):872-888.
[38]Hudson MP,Armstrong PW,Ruzyllo W,et al. Effects of selectivematrix metalloproteinase inhibitor(PG-116800)to prevent ventricularremodeling after myocardial infarction:results of the PREMIER(Pre-vention of Myocardial Infarction Early Remodeling)trial[J]. J AmColl Cardiol,2006,48(1):15-20.
[39]Cerisano G,Buonamici P,Valenti R,et al. Early short-term doxy-cycline therapy in patients with acute myocardial infarction and leftventricular dysfunction and the ominous progression to adverse remod-eling(TIPTOP). A randomized controlled trial[J]. J Am Coll Cardi-ol,2012,59(13):E349.
[40] Okamoto H, Imanaka-Yoshida K. Matricellular proteins:newmolecular targets to prevent heart failure[J]. Cardiovasc Ther,2012,30(4):e198-e209.
[41]Behfar A,Crespo-Diaz R,Terzic A,et al. Cell therapy for cardiacrepair-lessons from clinical trials[J]. Nat Rev Cardiol,2014,11(4):232-246.
[42]Qiu Y,Bayomy AF,Gomez MV,et al. A role for matrix stiffness inthe regulation of cardiac side population cell function[J]. Am J Phys-iol Heart Circ Physiol,2015,308(9):H990-H997.
[43]Chen WC,Wang Z,Missinato MA,et al. Decellularized zebrafishcardiac extracellular matrix induces mammalian heart regeneration[J]. Sci Adv,2016,2(11):e1600844.
[44]Wang J,Karra R,Dickson AL,et al. Fibronectin is deposited by in-jury-activated epicardial cells and is necessary for zebrafish heart re-generation[J]. Dev Biol,2013,382(2):427-435.
[45]Patterson NL,Iyer RP,de Castro Brás LE,et al. Using proteomics touncover extracellular matrix interactions during cardiac remodeling[J]. Proteomics Clin Appl,2013,7(7-8):516-527.
[46]Barallobrebarreiro J,Didangelos A,Schoendube FA,et al. Pro-teomics analysis of cardiac extracellular matrix remodeling in a porcinemodel of ischemia/reperfusion injury clinical perspective[J]. Circula-tion,2012,125(6):789-802.
[47]Deaguero JL,Mckown EN,Zhang L,et al. Altered protein levels inthe isolated extracellular matrix of failing human hearts with dilatedcardiomyopathy[J]. Cardiovasc Pathol,2017,26:12-20.
[48]Spinale FG,Zile MR. Integrating the myocardial matrix into heartfailure recognition and management[J]. Circ Res,2013,113(6):725-738.
[49]Lindsey ML,Hall ME,Harmancey R,et al. Adapting extracellularmatrix proteomics for clinical studies on cardiac remodeling post-myo-cardial infarction[J]. Clin Proteomics,2016,13(1):19.
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