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Open AccessJournal ArticleDOI

Biological activities of fibroblast growth factor-2 in the adult myocardium.

TLDR
An overview of current insights into the multiple roles of FGF-2 in the myocardium, as they pertain to two basic phenomena: ischemia-reperfusion injury and cardiac hypertrophy, is given.
Abstract
Fibroblast growth factor-2 (FGF-2) is a potent regulator of many cellular functions and phenomena, including cell proliferation, differentiation, survival, adhesion, migration, motility and apoptosis, and processes such as limb formation, wound healing, tumorigenesis, angiogenesis, vasculogenesis and blood vessel remodeling. In the adult myocardium, FGF-2 is expressed by various cell types, including cardiomyocytes, fibroblasts and smooth muscle cells. The biological effects of FGF-2 in the myocardium are mediated by the high-affinity tyrosine kinase receptor FGFR-1, the major FGF receptor in the heart. Here, we give an overview of current insights into the multiple roles of FGF-2 in the myocardium, as they pertain to two basic phenomena: ischemia-reperfusion injury and cardiac hypertrophy. The first category includes roles for FGF-2 in cardioprotection, the inflammatory response, angiogenesis and vascular remodeling, while the second includes myocyte hypertrophy, fibrosis, and gap junction functioning (conduction). Given the strong evidence for FGF-2 as both a cardioprotective and angiogenic agent, the therapeutic potential of FGF-2 in the ischemic myocardium is discussed.

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Journal ArticleDOI

The immune system and cardiac repair

TL;DR: Targeting inflammatory pathways following infarction may reduce cardiomyocyte injury and attenuate adverse remodeling, and understanding the role of the immune system in cardiac repair is necessary in order to design optimal strategies for cardiac regeneration.
OtherDOI

Pathophysiology of Myocardial Infarction.

TL;DR: The molecular signals and cellular effectors implicated in injury, repair, and remodeling of the infarcted heart, the mechanistic basis of the most common complications associated with myocardial infarction, and the pathophysiologic effects of established treatment strategies are described.
Journal ArticleDOI

Fibroblasts in myocardial infarction: a role in inflammation and repair

TL;DR: Considering their abundance, their crucial role in cardiac inflammation and repair, and their involvement in myocardial dysfunction and arrhythmogenesis, cardiac fibroblasts may be key therapeutic targets in cardiac remodeling.
References
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Journal ArticleDOI

Compensatory Enlargement of Human Atherosclerotic Coronary Arteries

TL;DR: It is concluded that human coronary arteries enlarge in relation to plaque area and that functionally important lumen stenosis may be delayed until the lesion occupies 40 percent of the internal elastic lamina area.
Journal ArticleDOI

Pathophysiology of ischaemia-reperfusion injury

TL;DR: The published literature in this field of investigation suggests that there are several potential targets for therapeutic intervention against I/R‐induced microvascular injury, and the protective effects of acute preconditioning are protein synthesis‐independent, while the effects of delayed preconditionsing require protein synthesis.
Book ChapterDOI

The FGF family of growth factors and oncogenes.

TL;DR: The FGF family includes seven members that share a varying degree of homology at the protein level and appear to have a similar broad mitogenic spectrum and promote the proliferation of a variety of cells of mesodermal and neuroectodermal origin.
Journal ArticleDOI

Biological roles of fibroblast growth factor-2.

TL;DR: Roles of FGF-2 in Development and Differentiation in Various Organ Systems and Mechanisms of Action: Extra- and Intracellular Signaling.
Journal ArticleDOI

Potent synergism between vascular endothelial growth factor and basic fibroblast growth factor in the induction of angiogenesis in vitro

TL;DR: It is demonstrated that like bFGF, VEGF induces an angiogenic response via a direct effect on endothelial cells, and that by acting in concert, these two cytokines have a potent synergistic effect on the induction of angiogenesis in vitro.
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