Targeting metalloproteinases in cardiac remodeling
Main Article Content
Abstract
During the last years metalloproteinases as a family of proteases have been implicated in various human diseases and catalytic mechanisms of pathological disorders. Metalloproteinases can be divided into two subgroups, matrix metalloproteinases (MMPs) and adamalysins (ADAMs). The MMPs consist of 6 basic subgroups which are inhibited by the tissue inhibitors of metalloproteinase (TIMP), while ADAMs consists of approximately 40 members. It is confirmed that metalloproteinases are an important factor for the cardiac remodeling process, interfering with the alteration of the cardiac structure induced by cardiac injury or increased haemodynamic load. The aim of this review is the analysis of the impact of metalloproteinases on cardiac remodeling and the factors affecting metalloproteinase activity. Metalloproteinases induce the remodeling process of the cardiac tissue in both beneficial and detrimental ways. TIMPs and various administered pharmacological agents may limit the effectiveness of metalloproteinases, therefore interfering in cardiac remodeling.
Downloads
Article Details
Copyright (c) 2019 Doxakis A, et al.
This work is licensed under a Creative Commons Attribution 4.0 International License.
Licensing and protecting the author rights is the central aim and core of the publishing business. Peertechz dedicates itself in making it easier for people to share and build upon the work of others while maintaining consistency with the rules of copyright. Peertechz licensing terms are formulated to facilitate reuse of the manuscripts published in journals to take maximum advantage of Open Access publication and for the purpose of disseminating knowledge.
We support 'libre' open access, which defines Open Access in true terms as free of charge online access along with usage rights. The usage rights are granted through the use of specific Creative Commons license.
Peertechz accomplice with- [CC BY 4.0]
Explanation
'CC' stands for Creative Commons license. 'BY' symbolizes that users have provided attribution to the creator that the published manuscripts can be used or shared. This license allows for redistribution, commercial and non-commercial, as long as it is passed along unchanged and in whole, with credit to the author.
Please take in notification that Creative Commons user licenses are non-revocable. We recommend authors to check if their funding body requires a specific license.
With this license, the authors are allowed that after publishing with Peertechz, they can share their research by posting a free draft copy of their article to any repository or website.
'CC BY' license observance:
|
License Name |
Permission to read and download |
Permission to display in a repository |
Permission to translate |
Commercial uses of manuscript |
|
CC BY 4.0 |
Yes |
Yes |
Yes |
Yes |
The authors please note that Creative Commons license is focused on making creative works available for discovery and reuse. Creative Commons licenses provide an alternative to standard copyrights, allowing authors to specify ways that their works can be used without having to grant permission for each individual request. Others who want to reserve all of their rights under copyright law should not use CC licenses.
Cohn J, Ferrari R, Sharpe N (2000) Cardiac remodeling—concepts and clinical implications: a consensus paper from an international forum on cardiac remodeling. JACC 35: 569-582. Link: https://bit.ly/2Mw1ult
Manso AM, Elsherif L, Min Kang S, Ross RS (2005) Integrins, membrane-type matrix metalloproteinases and ADAMs: Potential implications for cardiac remodeling. Cardiovasc Res 69: 574-584. Link: https://bit.ly/2YwtnMP
You Li Y, McTiernan C, Feldman A (2000) Interplay of matrix metalloproteinases, tissue inhibitors of metalloproteinases and their regulators in cardiac matrix remodeling. Cardiovasc Res 46: 214-224. Link: https://bit.ly/2Yh60eC
Bradham WS, Bozkurt B, Gunasinghe H, Mann D, Spinale FG (2002) Tumor necrosis factor-alpha and myocardial remodeling in progression of heart failure: a current perspective. Cardiovasc Res 53: 822-830. Link: https://bit.ly/2SSwtt8
Bujak M, Frangogiannis NG (2007) The role of TGF-β signaling in myocardial infarction and cardiac remodeling. Cardiovasc Res 74: 184-195. Link: https://bit.ly/2Yu36yp
Vanhoutte D, Schellings M, Pinto Y, Heymans S (2006) Relevance of matrix metalloproteinases and their inhibitors after myocardial infarction: A temporal and spatial window. Cardiovasc Res 69: 604-613. Link: https://bit.ly/2KeOiyO
Swynghedauw B (1999) Molecular Mechanisms of Myocardial Remodeling. APS 79: 215-262. Link: https://bit.ly/2YcFL9a
Ma Y, Castro Brás LE, Toba H, Padmanabhan R, Hall ME, et al. (2014) Myofibroblasts and the extracellular matrix network in post-MIcardiac remodeling. European Journal of Physiology. Link: https://bit.ly/316hnTS
Jun JH, Cho JE, Shim YH, Shim JK, Kwak YK (2011) Effects of propofol on the expression of matric metalloproteinases in rat cardiac fibroblasts after hypoxia and reoxygenation. Br J Anaesth 106: 650-658. Link: https://bit.ly/2Mw3iLh
Tian XF, Cui MX, Yang SW, Zhou YJ, Hu DY (2013) Cell death, dysglycemia and myocardial infarction. Biomedical Reports 1: 341-346. Link: https://bit.ly/2K8yj6F
Cuvelier A, Kuntz C, Sesboüé R, Muir JF, Martin JP (1997) Les métalloprotéinases de la matrice extracellulaire (MMP): structure et activité. Revue des Maladies Respiratoires 14: 1-10.
Newby AC, Pauschinger M, Spinale FG (2006) From tadpole tails to transgenic mice: Metalloproteinases have brought about a metamorphosis in our understanding of cardiovascular disease. Cardiovasc Res 69: 559-561. Link: https://bit.ly/2OqJ20a
Kandasamy AD, Chow AK, Ali M, Schulz R (2010) Matrix metalloproteinase-2 and myocardial oxidative stress injury: beyond the matrix.Cardiovasc Res 85: 413-423. Link: https://bit.ly/2GCgWJd
Janicki JS, Brower GL, Gardner JD, Forman MF, Stewart JA, et al. (2006) Cardiac mast cell regulation of matrix metalloproteinase-related ventricular remodeling in chronic pressure or volume overload. Cardiovasc Res 69: 657-665. Link: https://bit.ly/2Ow4Szr
Reinhardt D, Sigusch HH, Henβe J, Tyagi SC, Körfer R, et al. (2002) Cardiac remodelling in end stage heart failure: upregulation of matrix metalloproteinase (MMP) irrespective of the underlying disease, and evidence for a direct inhibitory effect of ACE inhibitors on MMP. Heart 88: 525-530. Link: https://bit.ly/2KieqZq
Jones CB, Sane DC, Herrington DM (2003) Matrix metalloproteinases: A review of their structure and role in acute coronary syndrome. Cardiovasc Res 59: 812-823. Link: https://bit.ly/2Yfrnxc
Nagase H, Visse R, Murphy G (2006) Structure and function of matrix metalloproteinases and TIMPs. Cardiovasc Res 69: 562-573. Link: https://bit.ly/2YBd993
Rutschow S, Li J, Schultheiss HP, Pauschinger M (2006) Myocardial proteases and matrix remodeling in inflammatory heart disease. Cardiovasc Res 69: 646-656. Link: https://bit.ly/2K3o7w2
Chow AK, Cena J, Schulz R (2007) Acute actions and novel targets of matrix metalloproteinases in the heart and vasculature. Br J Pharmacol 152: 189–205. Link: https://bit.ly/2yoqKSD
Brauer PR (2006) MMPs - Role in Cardiovascular Development and Disease. Frontiers in Bioscience 11: 447-478. Link: https://bit.ly/2K4io94
Spinale FG (2007) Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function. APS. 87: 1285-1342. Link: https://bit.ly/2K5KfWM
Sakata Y, Yamamoto K, Mano T, Nishikawa N, Yoshida J, et al. (2004) Activation of matrix metalloproteinases precedes left ventricular remodeling in hypertensive heart failure rats: its inhibition as a primary effect of Angiotensin-converting enzyme inhibitor. Circulation 109: 2143-2149. Link: https://bit.ly/2GFmMt9
Li MJ, Huang CX, Okello E, Yanhong T, Mohamed S (2009) Treatment with spironolactone for 24 weeks decreases the level of matrix metalloproteinases and improves cardiac function in patients with chronic heart failure of ischemic etiology. Can J Cardiol 25: 523–526. Link: https://bit.ly/2Ysbdjh
Nilsson L, Hallén J, Atar D, Jonasson L, Swahn E (2012) Early measurements of plasma matrix metalloproteinase-2 predict infarct size and ventricular dysfunction in ST-elevation myocardial infarction. Heart 98: 31-36. Link: https://bit.ly/2KeO22O
Sun Y (2009) Myocardial repair/remodelling following infarction: roles of local factors. Cardiovasc Res 81: 482-490. Link: https://bit.ly/2OvmXhc
Chancey AL, Brower GL, Peterson JT, Janicki JS (2002) Effects of matrix metalloproteinase inhibition on ventricular remodeling due to volume overload. Circulation 105: 1983-1988. Link: https://bit.ly/2YBbCjj
Webb Cs, Bonnema DD, Ahmed SH, Leonardi AH, McClure CD, et al. (2006) Specific Temporal Profile of Matrix Metalloproteinase Release Occurs in Patients After Myocardial Infarction: Relation to Left Ventricular Remodeling. Circulation 114: 1020-1027. Link: https://bit.ly/2YcpdON
Bergman MR, Teerlink JR, Mahimkar R, Li L, Zhu BQ, et al. (2007) Cardiac matrix metalloproteinase-2 expression independently induces marked ventricular remodeling and systolic dysfunction. Am J Physiol Heart Circ Physiol 292: 1847-1860. Link: https://bit.ly/2yrg5q4
Kelly D, Hkan S, Cockerill G, Ng LL, Thompson M, et al. (2008) Circulating Stromelysin-1 (MMP-3): A novel predictor of LV dysfunction, remodelling and all-cause mortality after acute myocardial infarction. Eur J Heart Fail 10: 133-139. Link: https://bit.ly/2MnV7Rj
Wei Y, Cui C, Lainscak M, Zhang X, Li J, et al. (2011) Type-specific dysregulation of matrix metalloproteinases and their tissue inhibitors in end-stage heart failure patients: relationship between MMP-10 and LV remodelling. Journal of Cellular and Molecular Medicine 15: 773–782. Link: https://bit.ly/316fB4Y
Peterson JT, Hallak H, Johnson L, Li H, O' Brien PM, et al. (2001) Matrix Metalloproteinase Inhibition Attenuates Left Ventricular Remodeling and Dysfunction in a Rat Model of Progressive Heart Failure. Circulation 103: 2303-2309. Link: https://bit.ly/2ytNIra
Lalu MM, Pasini E, Schulze CJ, Ferrari-Vivaldi M, Ferrari-Vivaldi G, et al. (2005) Ischaemia–reperfusion injury activates matrix metalloproteinases in the human heart. Eur Heart J 26: 27-35. Link: https://bit.ly/2YxF75C
Arndt Μ, Lendeckel U, Röcken C, Nepple K, Wolke C, et al. ((2002) Altered Expression of ADAMs (A Disintegrin And Metalloproteinase) in Fibrillating Human Atria. Circulation 105: 720-725. Link: https://bit.ly/2yrzya6
Berk BC, Fujiwara K, Lehoux S (2007) ECM remodeling in hypertensive heart disease. J Clin Invest 117: 568–575. Link: https://bit.ly/2LTbtSq
Briest W, Hölzl A, Raßler B, Deten A, Baba HA, et al. (2003) Significance of matrix metalloproteinases in norepinephrine-induced remodelling of rat hearts. Cardiovasc Res 57: 379-387. Link: https://bit.ly/2YlSsPn
Gupta SP (2012) Matrix Metalloproteinase Inhibitors: Specificity of Binding and Structure-Activity Relationships. London: Springer 9. Link: https://bit.ly/2KfStdG
Li H, Simon H, Bocan TMA, Peterson JT (2000) MMP/TIMP expression in spontaneously hypertensive heart failure rats: the effect of ACE- and MMP-inhibition. Cardiovasc Res 46: 298-306. Link: https://bit.ly/2K7lObs