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Cited by 301

The DOI matches its Crossref record; 19 of the 19 references it cites were found in a registry or an index.

Matrix Metalloproteinase Inhibition Attenuates Left Ventricular Remodeling and Dysfunction in a Rat Model of Progressive Heart Failure

Peterson, J. Thomas, Hallak, Hussein, Johnson, Linda, Li, Hua, O’Brien, Patrick M., Sliskovic, Drago R., Bocan, Thomas M. A., Coker, Mytsi L., Etoh, Takuma, Spinale, Francis G.·2001·Circulation
DOI 10.1161/01.cir.103.18.2303
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Abstract

Background—Matrix metalloproteinase (MMP) activation contributes to tissue remodeling in several disease states, and increased MMP activity has been observed in left ventricular (LV) failure. The present study tested the hypothesis that MMP inhibition would influence LV remodeling and function in developing LV failure. Methods and Results—LV size and function were measured in 5 groups of rats: (1) obese male spontaneously hypertensive heart failure rats (SHHF) at 9 months (n=10), (2) SHHF at 13 months (n=12), (3) SHHF rats treated with an MMP inhibitor during months 9 to 13 (PD166793 5 mg · kg−1· d−1 PO; n=14), (4) normotensive Wistar-Furth rats (WF) at 9 months (n=12), and (5) WF at 13 months (n=12). Plasma concentrations of the MMP inhibitor (116±11 μmol/L) reduced in vitro LV myocardial MMP-2 activity by ≈100%. LV function and geometry were similar in WF rats at 9 and 13 months. LV peak +dP/dt was unchanged at 9 months in SHHF but by 13 months was reduced in the SHHF group compared with WF (3578±477 versus 5983±109 mm Hg/s,P≤0.05). LV volume measured at an equivalent ex vivo pressure (10 mm Hg) was increased in SHHF at 9 months compared with WF (443±12 versus 563±33 mL,P≤0.05) and increased further by 13 months (899±64 mL,P≤0.05). LV myocardial MMP-2 activity was increased by ≈2-fold in SHHF at 9 and 13 months. With MMP inhibition, LV peak +dP/dt was similar to WF values and LV volume was reduced compared with untreated SHHF values (678±28 mL,P≤0.05). Conclusions—MMP activity contributes to LV dilation and progression to LV dysfunction in a rodent HF model, and direct MMP inhibition can attenuate this process.

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Metadata

Authors
Peterson, J. T., Hallak, H., Johnson, L., Li, H., O’Brien, P. M., Sliskovic, D. R., Bocan, T. M. A., Coker, M. L., Etoh, T., & Spinale, F. G.
Venue
Circulation
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2001-05-08
Volume
103
Issue
18
Pages
2303-2309
ISSN
  • 0009-7322 (ISSN-L)
  • 1524-4539
DOI
10.1161/01.cir.103.18.2303
OpenAlex
W1977660216
Cited by
301
References
19
FWCI
14.06
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Matrix Metalloproteinase Inhibition Attenuates Left Ventricular Remodeling and Dysfunction in a Rat Model of Progressive Heart Failure. https://app.cochat.ai/papers/10.1161/01.cir.103.18.2303
The paper
Peterson, J. T., Hallak, H., Johnson, L., Li, H., O’Brien, P. M., Sliskovic, D. R., Bocan, T. M. A., Coker, M. L., Etoh, T., & Spinale, F. G. (2001). Matrix Metalloproteinase Inhibition Attenuates Left Ventricular Remodeling and Dysfunction in a Rat Model of Progressive Heart Failure. Circulation. https://doi.org/10.1161/01.cir.103.18.2303

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.