Circulation Research. 2002;90:520-530
doi: 10.1161/01.RES.0000013290.12884.A3
doi: 10.1161/01.RES.0000013290.12884.A3
© 2002 American Heart Association, Inc.
Reviews |
Matrix Metalloproteinases
Regulation and Dysregulation in the Failing Heart
From the Medical University of South Carolina, Charleston.
Correspondence to Francis G. Spinale, MD, PhD, Cardiothoracic Surgery, Room 625, Strom Thurmond Research Building, 770 MUSC Complex, Medical University of South Carolina, 114 Doughty St, Charleston, SC 29425.
Abstract
Matrix metalloproteinases (MMPs) are a family of proteolytic enzymes responsible for myocardial extracellular protein degradation. Several MMP species identified within the human myocardium may be dysregulated in congestive heart failure (CHF). For example, MMPs that are expressed at very low levels in normal myocardium, such as collagenase-3 (MMP-13) and the membrane-type-1 MMPs, are substantially upregulated in CHF. However, MMP species are not uniformly increased in patients with end-stage CHF, suggesting that a specific portfolio of MMPs are expressed in the failing myocardium. With the use of animal models of CHF, a mechanistic relationship has been demonstrated with respect to myocardial MMP expression and the left ventricular (LV) remodeling process. The tissue inhibitors of the MMPs (TIMPs) are locally synthesized proteins that bind to active MMPs and thereby regulate net proteolytic activity. However, there does not appear to be a concomitant increase in myocardial TIMPs during the LV remodeling process and progression to CHF. This disparity between MMP and TIMP levels favors a persistent MMP activation state within the myocardium and likely contributes to the LV remodeling process in the setting of developing CHF. The elucidation of upstream signaling mechanisms that contribute to the selective induction of MMP species within the myocardium as well as strategies to normalize the balance between MMPs and TIMPs may yield some therapeutic strategies by which to control myocardial extracellular remodeling and thereby slow the progression of the CHF process.
Key Words: myocardial remodeling • heart failure • matrix metalloproteinases • matrix metalloproteinase inhibitors
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Z. Kassiri, G. Y. Oudit, O. Sanchez, F. Dawood, F. F. Mohammed, R. K. Nuttall, D. R. Edwards, P. P. Liu, P. H. Backx, and R. Khokha Combination of Tumor Necrosis Factor-{alpha} Ablation and Matrix Metalloproteinase Inhibition Prevents Heart Failure After Pressure Overload in Tissue Inhibitor of Metalloproteinase-3 Knock-Out Mice Circ. Res., August 19, 2005; 97(4): 380 - 390. [Abstract] [Full Text] [PDF]
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Q. Yu, R. R. Watson, J. J. Marchalonis, and D. F. Larson A role for T lymphocytes in mediating cardiac diastolic function Am J Physiol Heart Circ Physiol, August 1, 2005; 289(2): H643 - H651. [Abstract] [Full Text] [PDF]
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M. Pauschinger, S. Rutschow, K. Chandrasekharan, D. Westermann, A. Weitz, L. P. Schwimmbeck, H. Zeichhardt, W. Poller, M. Noutsias, J. Li, et al. Carvedilol improves left ventricular function in murine coxsackievirus-induced acute myocarditis Association with reduced myocardial interleukin-1{beta} and MMP-8 expression and a modulated immune response Eur J Heart Fail, June 1, 2005; 7(4): 444 - 452. [Abstract] [Full Text] [PDF]
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T. Ohtsuka, K. Inoue, Y. Hara, N. Morioka, K. Ohshima, J. Suzuki, A. Ogimoto, Y. Shigematsu, and J. Higaki Serum markers of angiogenesis and myocardial ultrasonic tissue characterization in patients with dilated cardiomyopathy Eur J Heart Fail, June 1, 2005; 7(4): 689 - 695. [Abstract] [Full Text] [PDF]
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A. Orlandi, A. Ciucci, A. Ferlosio, A. Pellegrino, L. Chiariello, and L. G. Spagnoli Increased Expression and Activity of Matrix Metalloproteinases Characterize Embolic Cardiac Myxomas Am. J. Pathol., June 1, 2005; 166(6): 1619 - 1628. [Abstract] [Full Text] [PDF]
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V. Lionetti, A. Linke, M. P. Chandler, M. E. Young, M. S. Penn, S. Gupte, C. d'Agostino, T. H. Hintze, W. C. Stanley, and F. A. Recchia Carnitine palmitoyl transferase-I inhibition prevents ventricular remodeling and delays decompensation in pacing-induced heart failure Cardiovasc Res, June 1, 2005; 66(3): 454 - 461. [Abstract] [Full Text] [PDF]
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N. Kawamura, T. Kubota, S. Kawano, Y. Monden, A. M. Feldman, H. Tsutsui, A. Takeshita, and K. Sunagawa Blockade of NF-{kappa}B improves cardiac function and survival without affecting inflammation in TNF-{alpha}-induced cardiomyopathy Cardiovasc Res, June 1, 2005; 66(3): 520 - 529. [Abstract] [Full Text] [PDF]
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M. Li, D. Georgakopoulos, G. Lu, L. Hester, D. A. Kass, J. Hasday, and Y. Wang p38 MAP Kinase Mediates Inflammatory Cytokine Induction in Cardiomyocytes and Extracellular Matrix Remodeling in Heart Circulation, May 17, 2005; 111(19): 2494 - 2502. [Abstract] [Full Text] [PDF]
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T. Ueland, A. Yndestad, E. Oie, G. Florholmen, B. Halvorsen, S. S. Froland, S. Simonsen, G. Christensen, L. Gullestad, and P. Aukrust Dysregulated Osteoprotegerin/RANK Ligand/RANK Axis in Clinical and Experimental Heart Failure Circulation, May 17, 2005; 111(19): 2461 - 2468. [Abstract] [Full Text] [PDF]
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M. L. Lindsey, D. K. Goshorn, C. E. Squires, G. P. Escobar, J. W. Hendrick, J. T. Mingoia, S. E. Sweterlitsch, and F. G. Spinale Age-dependent changes in myocardial matrix metalloproteinase/tissue inhibitor of metalloproteinase profiles and fibroblast function Cardiovasc Res, May 1, 2005; 66(2): 410 - 419. [Abstract] [Full Text] [PDF]
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J. Chen, C.-H. Tung, J. R. Allport, S. Chen, R. Weissleder, and P. L. Huang Near-Infrared Fluorescent Imaging of Matrix Metalloproteinase Activity After Myocardial Infarction Circulation, April 12, 2005; 111(14): 1800 - 1805. [Abstract] [Full Text] [PDF]
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R. A. Garcia, K. L. Brown, R. S. Pavelec, K. V. Go, J. W. Covell, and F. J. Villarreal Abnormal cardiac wall motion and early matrix metalloproteinase activity Am J Physiol Heart Circ Physiol, March 1, 2005; 288(3): H1080 - H1087. [Abstract] [Full Text] [PDF]
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J. D. Lovelock, A. H. Baker, F. Gao, J.-F. Dong, A. L. Bergeron, W. McPheat, N. Sivasubramanian, and D. L. Mann Heterogeneous effects of tissue inhibitors of matrix metalloproteinases on cardiac fibroblasts Am J Physiol Heart Circ Physiol, February 1, 2005; 288(2): H461 - H468. [Abstract] [Full Text] [PDF]
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S. Heymans, F. Lupu, S. Terclavers, B. Vanwetswinkel, J.-M. Herbert, A. Baker, D. Collen, P. Carmeliet, and L. Moons Loss or Inhibition of uPA or MMP-9 Attenuates LV Remodeling and Dysfunction after Acute Pressure Overload in Mice Am. J. Pathol., January 1, 2005; 166(1): 15 - 25. [Abstract] [Full Text] [PDF]
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J. S. Ikonomidis, J. W. Hendrick, A. M. Parkhurst, A. R. Herron, P. G. Escobar, K. B. Dowdy, R. E. Stroud, E. Hapke, M. R. Zile, and F. G. Spinale Accelerated LV remodeling after myocardial infarction in TIMP-1-deficient mice: effects of exogenous MMP inhibition Am J Physiol Heart Circ Physiol, January 1, 2005; 288(1): H149 - H158. [Abstract] [Full Text] [PDF]
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V. Franco, Y.-F. Chen, S. Oparil, J. A. Feng, D. Wang, F. Hage, and G. Perry Atrial Natriuretic Peptide Dose-Dependently Inhibits Pressure Overload-Induced Cardiac Remodeling Hypertension, November 1, 2004; 44(5): 746 - 750. [Abstract] [Full Text] [PDF]
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P. W.M. Fedak, D. S. Smookler, Z. Kassiri, N. Ohno, K. J. Leco, S. Verma, D. A.G. Mickle, K. L. Watson, C. V. Hojilla, W. Cruz, et al. TIMP-3 Deficiency Leads to Dilated Cardiomyopathy Circulation, October 19, 2004; 110(16): 2401 - 2409. [Abstract] [Full Text] [PDF]
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M. W.M. Schellings, Y. M. Pinto, and S. Heymans Matricellular proteins in the heart: possible role during stress and remodeling Cardiovasc Res, October 1, 2004; 64(1): 24 - 31. [Abstract] [Full Text] [PDF]
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S. Meiners, B. Hocher, A. Weller, M. Laule, V. Stangl, C. Guenther, M. Godes, A. Mrozikiewicz, G. Baumann, and K. Stangl Downregulation of Matrix Metalloproteinases and Collagens and Suppression of Cardiac Fibrosis by Inhibition of the Proteasome Hypertension, October 1, 2004; 44(4): 471 - 477. [Abstract] [Full Text] [PDF]
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Z. Xie, M. Singh, and K. Singh Differential Regulation of Matrix Metalloproteinase-2 and -9 Expression and Activity in Adult Rat Cardiac Fibroblasts in Response to Interleukin-1{beta} J. Biol. Chem., September 17, 2004; 279(38): 39513 - 39519. [Abstract] [Full Text] [PDF]
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