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Background Cardiac hypertrophy is an adaptive response of the heart to many cardio-vascular disorders including hypertension, infarction and defects of the valves. Elevated levels of cardiac cyclic guanosine-3’,5’-monophosphate (cGMP) activate cGMP-dependent protein kinase I (cGKI), which reportedly exhibited either anti-fibrotic and/or antihypertrophic effects or did not change the cardiac remodeling responses [1-5]. Based on these findings, we and others suggested that the ability of natriuretic peptides (NP) to oppose detrimental changes via cGMP/cGKI might strongly depend on the growth-promoting neurohormonal signals and stresses. Aiming to dissect the molecular details underlying cardiac cGMP signaling, we investigated the cysteine-rich LIM-only protein 4 (CRP4) as a novel target of cardio-vascular cGMP in vivo. CRP4 is phosphorylated at Ser-104 by cGMP/cGKI [6-8] and a highly related homologue of the muscle LIM protein CRP3/MLP, which has been linked to dilated and hypertrophic cardiomyopathies in mice and humans [9,10].

bmc pharmacology and toxicology

Cardiac cGMP/cGMP-dependent protein kinase I signalling requires cysteine-rich LIM-only protein 4 (CRP4) to oppose angiotensin II induced hypertrophy and fibrosis