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Cited by 435

The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.

Genetic and Pharmacological Inhibition of Galectin-3 Prevents Cardiac Remodeling by Interfering With Myocardial Fibrogenesis

Open access
Yu, Lili, Ruifrok, Willem P.T., Meissner, Maxi, Bos, Eelke M., van Goor, Harry, Sanjabi, Bahram, van der Harst, Pim, Pitt, Bertram, Goldstein, Irwin J., Koerts, Jasper A., van Veldhuisen, Dirk J., Bank, Ruud A., van Gilst, Wiek H., Silljé, Herman H.W., de Boer, Rudolf A.·2013·Circulation: Heart Failure

Abstract

Background—: Galectin-3 has been implicated in the development of organ fibrosis. It is unknown whether it is a relevant therapeutic target in cardiac remodeling and heart failure. Methods and Results—: Galectin-3 knock-out and wild-type mice were subjected to angiotensin II infusion (2.5 µg/kg for 14 days) or transverse aortic constriction for 28 days to provoke cardiac remodeling. The efficacy of the galectin-3 inhibitor N-acetyllactosamine was evaluated in TGR(mREN2)27 (REN2) rats and in wild-type mice with the aim of reversing established cardiac remodeling after transverse aortic constriction. In wild-type mice, angiotensin II and transverse aortic constriction perturbations caused left-ventricular (LV) hypertrophy, decreased fractional shortening, and increased LV end-diastolic pressure and fibrosis ( P <0.05 versus control wild type). Galectin-3 knock-out mice also developed LV hypertrophy but without LV dysfunction and fibrosis ( P =NS). In REN2 rats, pharmacological inhibition of galectin-3 attenuated LV dysfunction and fibrosis. To elucidate the beneficial effects of galectin-3 inhibition on myocardial fibrogenesis, cultured fibroblasts were treated with galectin-3 in the absence or presence of galectin-3 inhibitor. Inhibition of galectin-3 was associated with a downregulation in collagen production (collagen I and III), collagen processing, cleavage, cross-linking, and deposition. Similar results were observed in REN2 rats. Inhibition of galectin-3 also attenuated the progression of cardiac remodeling in a long-term transverse aortic constriction mouse model. Conclusions—: Genetic disruption and pharmacological inhibition of galectin-3 attenuates cardiac fibrosis, LV dysfunction, and subsequent heart failure development. Drugs binding to galectin-3 may be potential therapeutic candidates for the prevention or reversal of heart failure with extensive fibrosis.

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Metadata

Authors
Yu, L., Ruifrok, W. P. T., Meissner, M., Bos, E. M., van Goor, H., Sanjabi, B., van der Harst, P., Pitt, B., Goldstein, I. J., Koerts, J. A., van Veldhuisen, D. J., Bank, R. A., van Gilst, W. H., Silljé, H. H. W., & de Boer, R. A.
Venue
Circulation: Heart Failure
Published
2013-01
Volume
6
Issue
1
Pages
107-117
ISSN
  • 1941-3289 (ISSN-L)
  • 1941-3297
OpenAlex
W2161321429
Cited by
435
References
38
FWCI
18.42
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Genetic and Pharmacological Inhibition of Galectin-3 Prevents Cardiac Remodeling by Interfering With Myocardial Fibrogenesis. https://app.cochat.ai/papers/10.1161/circheartfailure.112.971168
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Yu, L., Ruifrok, W. P. T., Meissner, M., Bos, E. M., van Goor, H., Sanjabi, B., van der Harst, P., Pitt, B., Goldstein, I. J., Koerts, J. A., van Veldhuisen, D. J., Bank, R. A., van Gilst, W. H., Silljé, H. H. W., & de Boer, R. A. (2013). Genetic and Pharmacological Inhibition of Galectin-3 Prevents Cardiac Remodeling by Interfering With Myocardial Fibrogenesis. Circulation: Heart Failure. https://doi.org/10.1161/circheartfailure.112.971168

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

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