Ro 32‐3555, an orally active collagenase inhibitor, prevents cartilage breakdown <i>in vitro</i> and <i>in vivo</i>

Lewis, E. J.; Bishop, John D.; Bottomley, K. M. K.; Bradshaw, David J.; Brewster, Michael; Broadhurst, Michael J.; Brown, Paul A.; Budd, John M.; Elliott, Lucy H.; Greenham, A. K.; Johnson, William H.; Nixon, John; Rose, Felicity R. A. J.; Sutton, Blaine M.; Wilson, Kieran

doi:10.1038/sj.bjp.0701150

Cited by 128 publications

(54 citation statements)

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“…For these reasons, inhibition of MMPs has been considered as a new therapeutic approach to rheumatoid joint destruction (24). It has been reported that specific inhibition of individual MMPs has almost no effect in the treatment of murine arthritis, possibly due to another MMP compensation (30), but broad-spectrum MMP inhibition was shown to successfully reduce the clinical severity and cartilage destruction in a mouse model of RA (31,32). In our study, FRP inhibited the expression of MMP3, MMP9, and MMP13.…”

Section: Discussionmentioning

confidence: 99%

Ameliorative effects of follistatin‐related protein/TSC‐36/FSTL1 on joint inflammation in a mouse model of arthritis

Kawabata¹,

Tanaka²,

Fujii³

et al. 2004

Arthritis & Rheumatism

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Section: Discussionmentioning

confidence: 99%

Ameliorative effects of follistatin‐related protein/TSC‐36/FSTL1 on joint inflammation in a mouse model of arthritis

Kawabata¹,

Tanaka²,

Fujii³

et al. 2004

Arthritis & Rheumatism

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“…Because of their more selective activity profile and improved bioavailability than earlier compounds, in the present study, Ro 32-3555 and Ro 32-7315 were evaluated head to head in the infant rat model of PM with regard to their potential beneficial effects on structural brain damage and clinical and inflammatory parameters. The dosage used was adapted from earlier rodent studies (Roche Pharma, personal communication; [33][34][35].…”

mentioning

confidence: 99%

Matrix Metalloproteinase Inhibition Lowers Mortality and Brain Injury in Experimental Pneumococcal Meningitis

et al. 2014

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“…In arthritis, it was recently shown that the MMP inhibitor Ro32-3555 prevented cartilage breakdown in both rheumatoid arthritis and osteoarthritis in rats. 31 During dermal wound healing in rats, broad-range inhibition of MMP activity by ilomastat (GM6001) resulted in an enhanced wound strength that was associated with a decreased inflammatory response. 32 In thioglycollate-induced peritonitis in the mouse, ilomastat reduced the cellular infiltrate into the peritoneum.…”

Section: Mmps In Physiology and Diseasementioning

confidence: 99%

Matrix Metalloproteinase Inhibition After Myocardial Infarction

Creemers

Cleutjens

Smits

et al. 2001

Circulation Research

547

410

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Abstract-Increased activity of matrix metalloproteinases (MMPs) has been implicated in numerous disease processes, including tumor growth and metastasis, arthritis, and periodontal disease. It is now becoming increasingly clear that extracellular matrix degradation by MMPs is also involved in the pathogenesis of cardiovascular disease, including atherosclerosis, restenosis, dilated cardiomyopathy, and myocardial infarction. Administration of synthetic MMP inhibitors in experimental animal models of these cardiovascular diseases significantly inhibits the progression of, respectively, atherosclerotic lesion formation, neointima formation, left ventricular remodeling, pump dysfunction, and infarct healing. This review focuses on the role of MMPs in cardiovascular disease, in particular myocardial infarction and the subsequent progression to heart failure. MMPs, which are present in the myocardium and capable of degrading all the matrix components of the heart, are the driving force behind myocardial matrix remodeling. The recent finding that acute pharmacological inhibition of MMPs or deficiency in MMP-9 attenuates left ventricular dilatation in the infarcted mouse heart led to the proposal that MMP inhibitors could be used as a potential therapy for patients at risk for the development of heart failure after myocardial infarction. Although these promising results encourage the design of clinical trials with MMP inhibitors, there are still several unresolved issues. This review describes the biology of MMPs and discusses new insights into the role of MMPs in several cardiovascular diseases. Attention will be paid to the central role of the plasminogen system as an important activator of MMPs in the remodeling process after myocardial infarction. Finally, we speculate on the use of MMP inhibitors as potential therapy for heart failure. Key Words: myocardial infarction Ⅲ therapy Ⅲ matrix metalloproteinase inhibition M yocardial infarction (MI) leads to complex architectural alterations involving both the infarcted and noninfarcted myocardium. Dilatation of the left ventricle and infarct thinning, also called infarct expansion, are the most prominent structural changes in the infarct region. 1 Patients exhibiting extensive infarct expansion after MI are more likely to experience complications, such as the development of congestive heart failure, aneurysm formation, and myocardial rupture. 2 The extent of ventricular dilatation after MI is related to several factors such as the magnitude of the initial Original

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Ro 32‐3555, an orally active collagenase inhibitor, prevents cartilage breakdown in vitro and in vivo

Cited by 128 publications

References 30 publications

Ameliorative effects of follistatin‐related protein/TSC‐36/FSTL1 on joint inflammation in a mouse model of arthritis

Ameliorative effects of follistatin‐related protein/TSC‐36/FSTL1 on joint inflammation in a mouse model of arthritis

Matrix Metalloproteinase Inhibition Lowers Mortality and Brain Injury in Experimental Pneumococcal Meningitis

Matrix Metalloproteinase Inhibition After Myocardial Infarction

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