Galectin-3 marks activated macrophages in failure-prone hypertrophied hearts and contributes to cardiac dysfunction.
Umesh C. Sharma,Saraswati Pokharel,Thomas J. van Brakel,Jop H. van Berlo,Jack P.M. Cleutjens,Blanche Schroen,Sabine André,Harry J.G.M. Crijns,Hans J. Gabius,Jos G. Maessen,Yigal M. Pinto +10 more
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TL;DR: Galectin-3, a macrophage-derived mediator, induces cardiac fibroblast proliferation, collagen deposition, and ventricular dysfunction, which implies that HF therapy aimed at inflammatory responses may need to be targeted at the early stages of HF and probably needs to antagonize multiple inflammatory mediators, including galectIn-3.
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Abstract: Background— Inflammatory mechanisms have been proposed to be important in heart failure (HF), and cytokines have been implicated to add to the progression of HF. However, it is unclear whether such mechanisms are already activated when hypertrophied hearts still appear well-compensated and whether such early mechanisms contribute to the development of HF. Methods and Results— In a comprehensive microarray study, galectin-3 emerged as the most robustly overexpressed gene in failing versus functionally compensated hearts from homozygous transgenic TGRmRen2-27 (Ren-2) rats. Myocardial biopsies obtained at an early stage of hypertrophy before apparent HF showed that expression of galectin-3 was increased specifically in the rats that later rapidly developed HF. Galectin-3 colocalized with activated myocardial macrophages. We found galectin-3-binding sites in rat cardiac fibroblasts and the extracellular matrix. Recombinant galectin-3 induced cardiac fibroblast proliferation, collagen production, and cyclin D1...
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Citations
Macrophage depletion in hypertensive rats accelerates development of cardiomyopathy.
Harmen Reinier Zandbergen,Umesh C. Sharma,Sudhir Gupta,Johan W. Verjans,Susanne W.M. van den Borne,Saraswati Pokharel,Thomas J. van Brakel,Adriaan M. Duijvestijn,Nico van Rooijen,Jos G. Maessen,Chris P. M. Reutelingsperger,Yigal M. Pinto,Jagat Narula,Leonard Hofstra +13 more
TL;DR: It was showed that lack of macrophages was associated with earlier development of myocardial dysfunction in hypertensive rats, suggesting that modulation ofmacrophage function may be of value in the evolution of cardiomyopathy.
Dynamic Changes in Myocardial Matrix and Relevance to Disease: Translational Perspectives
TL;DR: This review discusses the complex dynamics of the cardiac ECM in the setting of myocardial infarction, pressure overload, and volume overload and the most current status of drugs under evaluation for use in cardiac fibrosis.
Galectin-3 is independently associated with cardiovascular mortality in community-dwelling older adults without known cardiovascular disease: The Rancho Bernardo Study
Lori B. Daniels,Paul Clopton,Gail A. Laughlin,Alan S. Maisel,Alan S. Maisel,Elizabeth Barrett-Connor +5 more
TL;DR: Higher levels of galectin-3 are independently associated with all-cause and CVD mortality among community-dwelling older adults with no known CVD at baseline.
Emerging biomarkers for acute heart conditions.
Vlad C. Vasile,Allan S. Jaffe +1 more
TL;DR: This study reviews several novel biomarkers – galectin-3, ST2 and copeptin, which are an active biomarker found in inflammatory and fibrotic processes and is a marker of mortality in acute cardiac conditions.
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Intracellular functions of galectins
TL;DR: This review summarizes the intracellular activities displayed by several galectins and discusses the possible underlying mechanisms.
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Extracellular functions of galectin-3
TL;DR: Galectin-3 has been suspected of modulating cell to extracellular matrix interactions in a novel fashion ever since it was first described but the rapid accumulation of research data in just the last 8 years alone has completely changed the perspective of this multifunctional protein.
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