Title
Molecular Mechanisms of Cardiac Hypertrophy and Heart Failure: Experimental Studies on Cardiac G ProteinCoupled Receptor Signal,Used
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Heart failure (HF) is a major cause of death worldwide. Remodeling of the heart plays an important role in the development of HF. Activiation of the vasoconstrictor endothelin1 (ET1) in HF has multiple adverse effects on the cardiovascular system. Dr. von Lueder et. al. identified the lungs as a major source of increased ET1 levels in a HF model. Pulmonary congestion increased the number of inflammatory cells as well as ET1 production. When HF animals were treated with a macrophage blocker in followup experiments, ET1 levels were reduced and, importantly, cardiac function improved. Important aspects of cardiac function are controlled by G proteincoupled receptors (GPCR). GPCR signaling is shut off by a small group of enzymes called GRKs. In geneticallyengineered mice (GRK3ct), GRK3 inhibition enhanced cardiac function, presumably through continuous aadrenergic signaling. Importantly, GRK3ct mice were prevented from HF when subjected to sustained severe cardiac stress for up to three months. The thesis by Lueder et. al. provides new mechanistic insights into the development of cardiac hypertrophy and HF and may yield novel therapeutic targets.
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