Research progress of collagen in cardiac remodeling after myocardial infarction

doi:10.3877/cma.j.issn.2095-655X.2024.01.004

Abstract

Abstract:

Myocardial collagen is the primary component of the extracellular matrix in the cardiomyocardium. It is responsible for maintaining the integrity of the heart structure and cardiomyocyte function and plays an important role in the change of cardiac function and cardiac remodeling after myocardial infarction. Myocardial infarction is a common cardiovascular disease, so it is essential to explore the function of collagen components after myocardial infarction. Myocardial collagen is affected by transforming growth factor-β1/Smads signaling pathway, neuroendocrine and a variety of regulatory molecules. Different types of collagen in the heart serve distinct functions to maintain the normal function of the heart. After myocardial infarction, most of the myocardial collagen exhibits increased expression. However, some collagen, specifically type V collagen, can contribute to an increase in scar area due to its decreasing consumption proportion. Therefore, maintaining an appropriate ratio of collagen is the precondition of maintaining normal heart function. The author reviews the functions of myocardial collagen, the alterations in myocardial collagen after myocardial infarction, the mechanisms of regulating changes in myocardial collagen, and the pharmaceutical interventions that can affect myocardial collagen.

Key words: Collagen, Myocardial infarction, Ventricular remodeling, Myocardial fibrosis, Signaling pathway

Xiaoyu Jiang, Di Fu, Xueying Chen, Cheng Shen, Lijun Gan. Research progress of collagen in cardiac remodeling after myocardial infarction[J]. Chinese Journal of Diagnostics(Electronic Edition), 2024, 12(01): 25-30.

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References 53

[1]	Lv S, Lu C, Li M, et al.The dynamic changes in myocardial collagen metabolism in experimental autoimmune myocarditis rats[J].Hellenic J Cardiol，2018，59(4)：234-237.DOI：10.1016/j.hjc.2017.12.006.
[2]	Ricard-Blum S．The collagen family[J].Cold Spring Harb Perspect Biol，2011，3(1)：a004978.DOI：10.1101/cshperspect.a004978.
[3]	Hanna A, Shinde AV, Li R, et al. Collagen denaturation in the infarcted myocardium involves temporally distinct effects of MT1-MMP-dependent proteolysis and mechanical tension[J].Matrix Biol，2021(99)：18-42.DOI：10.1016/j.matbio.2021.05.005.
[4]	Steffensen LB, Rasmussen LM.A role for collagen type IV in cardiovascular disease？[J].Am J Physiol Heart Circ Physiol，2018，315(3)：H610-H625.DOI：10.1152/ajpheart.00070.2018.
[5]	Rusu M, Hilse K, Schuh A, et al. Biomechanical assessment of remote and postinfarction scar remodeling following myocardial infarction[J].Sci Rep，2019，9(1)：16744.DOI：10.1038/s41598-019-53351-7.
[6]	Sadri G, Fischer AG, Brittian KR, et al.Collagen type XIX regulates cardiac extracellular matrix structure and ventricular function[J].Matrix Biol，2022(109)：49-69.DOI：10.1016/j.matbio.2022.03.007.
[7]	Singh D, Rai V, Agrawal DK.Regulation of collagen I and collagen III in tissue injury and regeneration[J].Cardiol Cardiovasc Med，2023，7(1)：5-16.DOI：10.26502/fccm.92920302.
[8]	Sudhakar A, Boosani CS. Signaling mechanisms of endogenous angiogenesis inhibitors derived from type IV collagen[J].Gene Regul Syst Bio，2007(1)：217-226.DOI：10.4137/grsb.s345.
[9]	Colorado PC, Torre A, Kamphaus G, et al.Anti-angiogenic cues from vascular basement membrane collagen[J].Cancer Res，2000，60(9)：2520-2526.
[10]	Yokota T, McCourt J, Ma F, et al.Type V collagen in scar tissue regulates the size of scar after heart injury[J].Cell，2020，182(3)：545-562.e23.DOI：10.1016/j.cell.2020.06.030.
[11]	Radhiga T, Senthil S, Sundaresan A, et al.Ursolic acid modulates MMPs，collagen-I，α-SMA，and TGF-β expression in isoproterenol-induced myocardial infarction in rats[J].Hum Exp Toxicol，2019，38(7)：785-793.DOI：10.1177/0960327119842620.
[12]	Frangogiannis NG.Pathophysiology of myocardial infarction[J].Compr Physiol，2015，5(4)：1841-1875.DOI：10.1002/cphy.c150006.
[13]	Yang HX, Xu GR, Zhang C, et al.The aqueous extract of Gentianella acuta improves isoproterenol-induced myocardial fibrosis via inhibition of the TGF-β1/Smads signaling pathway[J].Int J Mol Med，2020，45(1)：223-233.DOI：10.3892/ijmm.2019.4410.
[14]	Li J, Ge F, Wuken S, et al.Zerumbone，a humulane sesquiterpene from Syringa pinnatifolia，attenuates cardiac fibrosis by inhibiting of the TGF-β1/Smad signaling pathway after myocardial infarction in mice[J].Phytomedicine，2022(100)：154078.DOI：10.1016/j.phymed.2022.154078.
[15]	Venugopal H, Hanna A, Humeres C, et al.Properties and functions of fibroblasts and myofibroblasts in myocardial infarction[J].Cells，2022，11(9)：1386.DOI：10.3390/cells11091386.
[16]	Gao L, Wang LY, Liu ZQ, et al.TNAP inhibition attenuates cardiac fibrosis induced by myocardial infarction through deactivating TGF-β1/Smads and activating P53 signaling pathways[J].Cell Death Dis，2020，11(1)：44.DOI：10.1038/s41419-020-2243-4.
[17]	Kuhn TC, Knobel J, Burkert-Rettenmaier S, et al.Secretome analysis of cardiomyocytes identifies PCSK6 (proprotein convertase subtilisin/kexin type (6) as a novel player in cardiac remodeling after myocardial infarction[J].Circulation，2020，141(20)：1628-1644.DOI：10.1161/CIRCULATIONAHA.119.044914.
[18]	Schumacher D, Alampour-Rajabi S, Ponomariov V, et al.Cardiac FGF23：new insights into the role and function of FGF23 after acute myocardial infarction[J].Cardiovasc Pathol，2019(40)：47-54.DOI：10.1016/j.carpath.2019.02.001.
[19]	Pollard CM, Desimine VL, Wertz SL, et al.Deletion of osteopontin enhances β-adrenergic receptor-dependent anti-fibrotic signaling in cardiomyocytes[J].Int J Mol Sci，2019，20(6)：1396.DOI：10.3390/ijms20061396.
[20]	Du Y, Demillard LJ, Ren J．Catecholamine-induced cardiotoxicity：a critical element in the pathophysiology of stroke-induced heart injury[J].Life Sci，2021(287)：120106.DOI：10.1016/j.lfs.2021.120106.
[21]	Wu Y, Liu Y, Pan Y, et al.MicroRNA-135a inhibits cardiac fibrosis induced by isoproterenol via TRPM7 channel[J].Biomed Pharmacother，2018(104)：252-260.DOI：10.1016/j.biopha.2018.04.157.
[22]	Hu G, Ding X, Gao F, et al.Calcium and integrin binding protein 1 (CIB1) induces myocardial fibrosis in myocardial infarction via regulating the PI3K/Akt pathway[J].Exp Anim，2022，71(1)：1-13.DOI：10.1538/expanim.21-0063.
[23]	Zhang H, Zhang P, Long CD, et al.m6A methyltransferase METTL3 promotes retinoblastoma progression via PI3K/AKT/mTOR pathway[J].J Cell Mol Med，2020，24(21)：12368-12378.DOI：10.1111/jcmm.15736.
[24]	Meng F, Liu Y, Chen Q, et al.METTL3 contributes to renal ischemia-reperfusion injury by regulating Foxd1 methylation[J].Am J Physiol Renal Physiol，2020，319(5)：F839-F847.DOI：10.1152/ajprenal.00222.2020.
[25]	Song H, Song SX, Cheng M, et al.METTL3-mediated m6A RNA methylation promotes the anti-tumour immunity of natural killer cells [J].Nat Commun，2021，12(1)：5522.DOI：10.1038/s41467-021-25803-0.
[26]	Wang H, Xu B, Shi J．N6-methyladenosine METTL3 promotes the breast cancer progression via targeting Bcl-2[J].Gene，2020(722)：144076.DOI：10.1016/j.gene.2019.144076.
[27]	Lee H, Bao S, Qian Y, et al.Stage-specific requirement for Mettl3-dependent m(6)A mRNA methylation during haematopoietic stem cell differentiation[J].Nat Cell Biol，2019，21(6)：700-709.DOI：10.1038/s41556-019-0318-1.
[28]	Li XZ, Yuan BC, Lu M, et al.The methyltransferase METTL3 negatively regulates nonalcoholic steatohepatitis (NASH) progression[J].Nat Commun，2021，12(1)：7213.DOI：10.1038/s41467-021-27539-3.
[29]	Wang X, Li Y, Li J, et al.Mechanism of METTL3-mediated m(6)A modification in cardiomyocyte pyroptosis and myocardial ischemia-reperfusion injury[J].Cardiovasc Drugs Ther，2023，37(3)：435-448.DOI：10.1007/s10557-021-07300-0.
[30]	Zhao K, Yang C, Zhang J, et al.METTL3 improves cardiomyocyte proliferation upon myocardial infarction via upregulating miR-17-3p in a DGCR8-dependent manner[J].Cell Death Disco，2021，7(1)：291.DOI：10.1038/s41420-021-00688-6.
[31]	Dorn LE, Lasman L, Chen J, et al.The N(6)-methyladenosine mRNA methylase METTL3 controls cardiac homeostasis and hypertrophy[J].Circulation，2019，139(4)：533-545.DOI：10.1161/CIRCULATIONAHA.118.036146.
[32]	Li T, Zhuang Y, Yang W, et al. Silencing of METTL3 attenuates cardiac fibrosis induced by myocardial infarction via inhibiting the activation of cardiac fibroblasts[J].FASEB J，2021，35(2)：e21162.DOI：10.1096/fj.201903169R.
[33]	Li G, Zhao C, Fang S．SGLT2 promotes cardiac fibrosis following myocardial infarction and is regulated by miR-141[J].Exp Ther Med，2021，22(1)：715.DOI：10.3892/etm.2021.10147.
[34]	Wang C, Zhang C, Liu L, et al.Macrophage-derived mir-155-containing exosomes suppress fibroblast proliferation and promote fibroblast inflammation during cardiac injury[J].Mol Ther，2017，25(1)：192-204.DOI：10.1016/j.ymthe.2016.09.001.
[35]	Li Y, Duan JZ, He Q, et al. miR-155 modulates high glucose-induced cardiac fibrosis via the Nrf2/HO-1 signaling pathway[J].Mol Med Rep，2020，22(5)：4003-4016.DOI：10.3892/mmr.2020.11495.
[36]	Wang X, Khalil RA.Matrix metalloproteinases，vascular remodeling，and vascular disease[J].Adv Pharmacol，2018(81)：241-330.DOI：10.1016/bs.apha.2017.08.002.
[37]	Bayrakci N, Özkan G, Akpinar S, et al.Procollagen C-proteinase enhancer-1 and renal failure in multiple myeloma[J].Int Urol Nephrol，2022，54(11)：3033-3038.DOI：10.1007/s11255-022-03378-z.
[38]	Lagoutte P, Bettler E, Vadon-Le Goff S, et al. Procollagen C-proteinase enhancer-1 (PCPE-1)，a potential biomarker and therapeutic target for fibrosis[J].Matrix Biol Plus，2021(11)：100062.DOI：10.1016/j.mbplus.2021.100062.
[39]	Reichert K, Pereira do Carmo HR, Galluce Torina A, et al.Atorvastatin improves ventricular remodeling after myocardial infarction by interfering with collagen metabolism[J].PLoS One，2016，11(11)：e0166845.DOI：10.1371/journal.pone.0166845.
[40]	Li X, Wang G, Qi LM, et al.Aspirin reduces cardiac interstitial fibrosis by inhibiting Erk1/2-Serpine 2 and P-Akt signalling pathways[J].Cell Physiol Biochem，2018，45(5)：1955-1965.DOI：10.1159/000487972.
[41]	Zhang Y, Lin X, Chu Y, et al.Dapagliflozin：a sodium-glucose cotransporter 2 inhibitor，attenuates angiotensin II-induced cardiac fibrotic remodeling by regulating TGFβ1/Smad signaling[J].Cardiovasc Diabetol，2021，20(1)：121.DOI：10.1186/s12933-021-01312-8.
[42]	Ma J, Yin C, Ma S, et al.Shensong Yangxin capsule reduces atrial fibrillation susceptibility by inhibiting atrial fibrosis in rats with post-myocardial infarction heart failure[J].Drug Des Devel Ther，2018(12)：3407-3418.DOI：10.2147/DDDT.S182834.
[43]	Ma S, Ma J, Guo L, et al.Tongguan capsule-derived herb reduces susceptibility to atrial fibrillation by inhibiting left atrial fibrosis via modulating cardiac fibroblasts[J].J Cell Mol Med，2019，23(2)：1197-1210.DOI：10.1111/jcmm.14022.
[44]	Yang Y, Li J, Rao T, et al.The role and mechanism of hyperoside against myocardial infarction in mice by regulating autophagy via NLRP1 inflammation pathway[J].J Ethnopharmacol，2021(276)：114187.DOI：10.1016/j.jep.2021.114187.
[45]	Tan Z, Jiang X, Zhou W, et al.Taohong siwu decoction attenuates myocardial fibrosis by inhibiting fibrosis proliferation and collagen deposition via TGFBR1 signaling pathway[J].J Ethnopharmacol，2021(270)：113838.DOI：10.1016/j.jep.2021.113838.
[46]	Li X, Xiang N, Wang Z．Ginsenoside Rg2 attenuates myocardial fibrosis and improves cardiac function after myocardial infarction via AKT signaling pathway[J].Biosci Biotechnol Biochem，2020，84(11)：2199-2206.DOI：10.1080/09168451.2020.1793292.
[47]	Li M, Tan H, Gao T, et al.Gypensapogenin I ameliorates isoproterenol (ISO)-induced myocardial damage through regulating the TLR4/NF-κB/NLRP3 pathway[J].Molecules，2022，27(16).DOI：10.3390/molecules27165298.
[48]	Yang J, Wang B, Li N, et al.Salvia miltiorrhiza and carthamus tinctorius extract prevents cardiac fibrosis and dysfunction after myocardial infarction by epigenetically inhibiting Smad3 expression[J].Evid Based Complement Alternat Med，2019(2019)：6479136.DOI：10.1155/2019/6479136.
[49]	Ni T, Huang X, Pan S, et al.Dihydrolycorine attenuates cardiac fibrosis and dysfunction by downregulating runx1 following myocardial infarction[J].Oxid Med Cell Longev，2021(2021)：8528239.DOI：10.1155/2021/8528239.
[50]	Zhang G, Zhang X, Li D, et al.Long-term oral atazanavir attenuates myocardial infarction-induced cardiac fibrosis[J].Eur J Pharmacol，2018(828)：97-102.DOI：10.1016/j.ejphar.2018.03.041.
[51]	Chen P, Zhou D, Liu Y, et al.Peiminine inhibits myocardial injury and fibrosis after myocardial infarction in rats by regulating mitogen-activated protein kinase pathway[J].Korean J Physiol Pharmacol，2022，26(2)：87-94.DOI：10.4196/kjpp.2022.26.2.87.
[52]	Gallet R, Dawkins J, Valle J, et al.Exosomes secreted by cardiosphere-derived cells reduce scarring，attenuate adverse remodelling，and improve function in acute and chronic porcine myocardial infarction[J].Eur Heart J，2017，38(3)：201-211.DOI：10.1093/eurheartj/ehw240.
[53]	Jung M, Ma YG, Iyer RP, et al.IL-10 improves cardiac remodeling after myocardial infarction by stimulating M2 macrophage polarization and fibroblast activation[J].Basic Res Cardiol，2017，112(3)：33.DOI：10.1007/S00395-017-0622-5.

药物种类	药物名称	调节的胶原类型	调节相关的因子	参考文献
心血管常用药物	阿托伐他汀	Ⅰ型胶原水平下调	抑制IL-1表达	[39]
	阿司匹林	Ⅰ型胶原水平下调	抑制TGF-β1的表达	[40]
	达格列净	抑制胶原沉积	负性调节TGF-β1/Smad信号通路	[41]
中成药及天然药物提取物	参松养心胶囊	抑制Ⅰ、Ⅲ型胶原表达	下调TGF-β1、MMP-9、TIMP-Ⅰ	[42]
	通冠胶囊	抑制Ⅰ、Ⅲ型胶原表达	降低TGF-β1、MMP-9表达	[43]
	金丝桃苷	减轻纤维蛋白原沉积	IL-1β的表达下降	[44]
	桃红四物汤	抑制Ⅰ、Ⅲ型胶原表达	降低TGF-βR1、Smad2/3磷酸化	[45]
	Zerumbone	降低Ⅰ、Ⅲ型胶原的水平	TGF-β1、P-Smad2、P-Smad3表达下调，Smad7表达上调	[14]
	人参皂苷Rg2	降低Ⅰ、Ⅲ型胶原的水平	心肌梗死后AKT通路被显著抑制	[46]
	达马烷型皂苷元I	减轻胶原沉积	抑制IL-1β和IL-18	[47]
	丹参红花提取物	降低Ⅰ、Ⅲ型胶原的表达水平	降低Smad3	[48]
	二水石蒜碱	Ⅰ型胶原下调	TGF-β和P-Smad3下调	[49]
抗病毒药	阿扎那韦	降低Ⅰ、Ⅲ型胶原	下调HMGB1、TLR9和抑制核因子κB磷酸化	[50]
血尿酸抑制剂	培米宁	抑制Ⅰ、Ⅲ型胶原表达	抑制IL-1β、IL-6和TNF-α水平升高	[51]
其他类型药物	心肌球来源细胞外泌体	瘢痕明显减小	－	[52]
	IL-10	Ⅰ、Ⅲ型胶原分泌减少	降低透明质酸酶3	[53]

药物种类	药物名称	调节的胶原类型	调节相关的因子	参考文献
心血管常用药物	阿托伐他汀	Ⅰ型胶原水平下调	抑制IL-1表达	[39]
	阿司匹林	Ⅰ型胶原水平下调	抑制TGF-β1的表达	[40]
	达格列净	抑制胶原沉积	负性调节TGF-β1/Smad信号通路	[41]
中成药及天然药物提取物	参松养心胶囊	抑制Ⅰ、Ⅲ型胶原表达	下调TGF-β1、MMP-9、TIMP-Ⅰ	[42]
	通冠胶囊	抑制Ⅰ、Ⅲ型胶原表达	降低TGF-β1、MMP-9表达	[43]
	金丝桃苷	减轻纤维蛋白原沉积	IL-1β的表达下降	[44]
	桃红四物汤	抑制Ⅰ、Ⅲ型胶原表达	降低TGF-βR1、Smad2/3磷酸化	[45]
	Zerumbone	降低Ⅰ、Ⅲ型胶原的水平	TGF-β1、P-Smad2、P-Smad3表达下调，Smad7表达上调	[14]
	人参皂苷Rg2	降低Ⅰ、Ⅲ型胶原的水平	心肌梗死后AKT通路被显著抑制	[46]
	达马烷型皂苷元I	减轻胶原沉积	抑制IL-1β和IL-18	[47]
	丹参红花提取物	降低Ⅰ、Ⅲ型胶原的表达水平	降低Smad3	[48]
	二水石蒜碱	Ⅰ型胶原下调	TGF-β和P-Smad3下调	[49]
抗病毒药	阿扎那韦	降低Ⅰ、Ⅲ型胶原	下调HMGB1、TLR9和抑制核因子κB磷酸化	[50]
血尿酸抑制剂	培米宁	抑制Ⅰ、Ⅲ型胶原表达	抑制IL-1β、IL-6和TNF-α水平升高	[51]
其他类型药物	心肌球来源细胞外泌体	瘢痕明显减小	－	[52]
	IL-10	Ⅰ、Ⅲ型胶原分泌减少	降低透明质酸酶3	[53]

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