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L-Arginine at the Crossroads of Biochemical Pathways Involved in Myocardial Hypertrophy

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Book cover Signal Transduction and Cardiac Hypertrophy

Summary

Both ornithine decarboxylase (ODC) and nitric oxide synthase (NOS) activities rely on the availability of the common substrate L-arginine, which is directly processed by NOS to nitric oxide (NO) and L-citrulline. Alternatively, arginine is acted on by arginase in the urea cycle to produce ornithine, which then enters polyamine biosynthesis. Evidence in the literature points out that NO is able to inhibit ODC and polyamines can inhibit NOS. Both of these observations seem to indicate that the two metabolic pathways may crosstalk in regulating complex organic functions and the heart is a possible target organ for this interplay. It has been demonstrated that upregulation of ODC activity is critical in the hypertrophic myocardial response, which is also consistent with observations involving conditions of nitric oxide deficiency.

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Giordano, E., Shantz, L.M., Hillary, R.A., Guarnieri, C., Caldarera, C.M., Pegg, A.E. (2003). L-Arginine at the Crossroads of Biochemical Pathways Involved in Myocardial Hypertrophy. In: Dhalla, N.S., Hryshko, L.V., Kardami, E., Singal, P.K. (eds) Signal Transduction and Cardiac Hypertrophy. Progress in Experimental Cardiology, vol 7. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0347-7_4

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