The Publication:

Effects of emodin, a plant-derived anthraquinone, on TGF-β1-induced cardiac fibroblast activation and function

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Publication Summary:

Cardiac fibrosis is a condition characterized by an abnormal thickening of the heart valves and muscles due to the accumulation of excess extracellular matrix, mainly composed of fibrous connective tissue. This process is often a response to damage or stress such as hypertension, heart attack, or certain inflammatory diseases. Fibrosis occurs when the body attempts to repair cardiac damage but does so in an excessive or unregulated manner. When fibrotic tissue replaces normal heart tissue, it can disrupt the heart's electrical conduction system and impair the heart's ability to pump blood effectively, potentially leading to heart failure, arrhythmias, and other serious cardiovascular complications. The signaling networks leading to cardiac fibrosis are complex, contributing to the general lack of progress in developing effective therapy to prevent or reverse this condition. Several studies have shown protective effects of emodin, a plant-derived anthraquinone, in animal models of fibrosis, but question remains regarding how emodin attenuates fibrosis. Transforming growth factor beta 1 (TGF-β1) is a potent stimulus of fibrosis and fibroblast activation. In this study, we evaluated the effects of emodin on activation and function of cardiac fibroblasts following treatment with TGF-β1. We demonstrate that emodin attenuates TGF-β1-induced fibroblast activation and collagen accumulation in cultured cells. Emodin inhibited activation of several canonical (SMAD2/3) and noncanonical (Erk1/2) TGF-β signaling pathways. These results suggest that emodin may be further developed as an effective therapeutic agent for cardiac fibrosis.