cGKI signaling in cardiac hypertrophy

cGKI signaling in cardiac hypertrophy

The atrial natriuretic peptide (ANP) has been shown to modulate hypertrophy of the heart via the cardiac NP receptor guanylyl cyclase-A (GC-A) [1]. Also, analysis of transgenic mice with a cardiomyocyte (cM) specific overexpression of GC-A and the chronic inhibition of the cGMP-degrading phosphodiesterase-5 by sildenafil indicated that the second messenger cGMP can blunt hypertrophic signals fr...

Reply to Kass and Takimoto: Cardiac hypertrophy without cGKI and PDE5 in cardiac myocytes

Concerning the letter by Kass and Takimoto (1) in PNAS regarding our recent publication (2), we would like to make the following comments. First, we agree that our results showing a “lack of importance” for cGMP-dependent protein kinase I (cGKI) as a modulator of cardiac hypertrophy only refers to the “basal” condition as we clearly stated in the manuscript (1, 2). We purposely did not use guan...

Calcineurin signaling in human cardiac hypertrophy.

The initial observation in 19981 that calcineurin, a calmodulin-dependent protein phosphatase, is capable of driving cardiac hypertrophy, heart failure, and death in experimental animal models received special attention for several reasons. Previous evidence suggested that dysregulation of calcium metabolism is an integral feature of stresses that promote hypertrophy, and calcineurin was known ...

cGKI and vascular restenosis 1 Role of smooth muscle cGMP/cGKI signaling in murine vascular restenosis

Ras, PI3-kinase and mTOR signaling in cardiac hypertrophy.

Cardiac hypertrophy involves increased mass (growth) of the heart and a cardinal feature of this condition is increased rates of protein synthesis. Several signaling pathways have been implicated in cardiac hypertrophy including the phosphatidylinositol 3-kinase (PI3K) and Ras/Raf/MEK/Erk pathways. PI3K lies upstream of the mammalian target of rapamycin (mTOR), an important positive regulator o...