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C ardiac fibrosis is a hallmark of cardiomyocyte death during heart disease progression and considered to be both a cause and a result of heart failure. It is characterized by excessive growth of interstitial fibroblasts and collagen deposition in the myocardium, which initially contributes to an increase of cardiac stiffness and subsequent diastolic dysfunction, but eventually leads to contractile dysfunction. The initiation of cardiac fibrosis is cardiomyocyte death or other stimuli such as cytokine production, followed by infiltration of inflammatory cells and subsequent replacement with proliferating fibroblasts and collagen fibers. Since the extent of fibrotic area is correlated with the degree of contractile dysfunction and frequency of premature death by heart failure or lethal arrhythmia, efforts have been focused on the attenuation of the fibrosis. Prostaglandins (PGs) are physiologically active lipid compounds synthesized from arachidonic acids. The name prostaglandin derives from the prostate gland where it was first isolated by V. Euler in 1935 3) but it is produced by almost all nucleated cells. Until now, more than 10 types of prostaglandins have been discovered. Among them, prostaglandin E2 (PGE2) has been well studied, especially in inflammatory cells, and is also known to be the predominant type of PGs in solid tumors, skin, and left ventricular cardiomyocytes. PGE2 has versatile biological effects in many organs, which depend on the activation of its prostanoid EP receptors, of which there are 4 subtypes, EP1, EP2, EP3, and EP4. These are the 7-transmembrane G protein-coupled receptors expressed on vascular smooth muscle cells, vascular endothelial cells, cardiac fibroblasts, and cardiomyocytes in the context of the heart organ. Despite intensive investigation of PGE2 signaling in the heart, there still remains controversy as to whether the functional outcome of the PGE2-EPs axis is beneficial or maladaptive. The reasons behind this are that it shares variable downstream targets such as Gior Gs-type G-proteins, and the redundancy of each EP. Nevertheless, PGE2-EPs signaling plays important roles in the pathophysiological aspects of heart disease.

Prostaglandin E2 Signaling as a Target of Anti-Cardiac Fibrosis in Heart Failure Treatment