Polyamine metabolism and the hypertrophic heart

Lisa Shantz, Emanuele Giordano

Research output: Chapter in Book/Report/Conference proceedingChapter

4 Citations (Scopus)

Abstract

Cardiac muscle hypertrophy is one of the most important compensatory responses of the heart to multiple stresses that may be placed on it. If the stress is not relieved, sustained hypertrophy may progress to dysfunction and heart failure. The polyamines putrescine, spermidine, and spermine increase within hours of various types of experimentally induced cardiac hypertrophy, along with ornithine decarboxylase (ODC) gene expression. Several animal models have implicated ODC induction as an important factor in the development of hypertrophy, particularly in response to β-adrenergic stimulation. Novel transgenic mouse lines that overexpress several enzymes of polyamine metabolism in the heart have been generated in recent years, and crosses of these lines have pointed to decarboxylated adenosylmethionine and its control by S-adenosylmethionine decarboxylase as another important element in maintaining cardiac polyamine homeostasis. The activity of arginase is thought to play a regulatory role in the biosynthesis of both nitric oxide (NO) and polyamines, and NO deficiency has been linked to the development of cardiac hypertrophy. Genetically altered mouse lines with changes in arginine and NO metabolism in the heart are available, many of which possess cardiac abnormalities. These models will provide a valuable means to address the interdependence of arginine and ornithine metabolism in the development of myocardial hypertrophy and failure. Use of these tools may lead to a better understanding of the control of the signaling pathways that include the polyamines, arginine, and NO, allowing future work to focus on the interactions between these pathways in the development of heart disease.

Original languageEnglish (US)
Title of host publicationPolyamine Cell Signaling
Subtitle of host publicationPolyamine Cell Signaling
PublisherHumana Press
Pages123-137
Number of pages15
ISBN (Print)9781588296252
DOIs
StatePublished - Dec 1 2006

Fingerprint

Polyamines
Metabolism
Nitric Oxide
Cardiomegaly
Hypertrophy
Ornithine Decarboxylase
Arginine
Heart Failure
Adenosylmethionine Decarboxylase
Arginase
Ornithine
Putrescine
Spermidine
Spermine
Adrenergic Agents
Transgenic Mice
Biosynthesis
Heart Diseases
Myocardium
Homeostasis

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Shantz, L., & Giordano, E. (2006). Polyamine metabolism and the hypertrophic heart. In Polyamine Cell Signaling: Polyamine Cell Signaling (pp. 123-137). Humana Press. https://doi.org/10.1007/978-1-59745-145-1_7
Shantz, Lisa ; Giordano, Emanuele. / Polyamine metabolism and the hypertrophic heart. Polyamine Cell Signaling: Polyamine Cell Signaling. Humana Press, 2006. pp. 123-137
@inbook{75e323243b30451c837e1e86ffecbe77,
title = "Polyamine metabolism and the hypertrophic heart",
abstract = "Cardiac muscle hypertrophy is one of the most important compensatory responses of the heart to multiple stresses that may be placed on it. If the stress is not relieved, sustained hypertrophy may progress to dysfunction and heart failure. The polyamines putrescine, spermidine, and spermine increase within hours of various types of experimentally induced cardiac hypertrophy, along with ornithine decarboxylase (ODC) gene expression. Several animal models have implicated ODC induction as an important factor in the development of hypertrophy, particularly in response to β-adrenergic stimulation. Novel transgenic mouse lines that overexpress several enzymes of polyamine metabolism in the heart have been generated in recent years, and crosses of these lines have pointed to decarboxylated adenosylmethionine and its control by S-adenosylmethionine decarboxylase as another important element in maintaining cardiac polyamine homeostasis. The activity of arginase is thought to play a regulatory role in the biosynthesis of both nitric oxide (NO) and polyamines, and NO deficiency has been linked to the development of cardiac hypertrophy. Genetically altered mouse lines with changes in arginine and NO metabolism in the heart are available, many of which possess cardiac abnormalities. These models will provide a valuable means to address the interdependence of arginine and ornithine metabolism in the development of myocardial hypertrophy and failure. Use of these tools may lead to a better understanding of the control of the signaling pathways that include the polyamines, arginine, and NO, allowing future work to focus on the interactions between these pathways in the development of heart disease.",
author = "Lisa Shantz and Emanuele Giordano",
year = "2006",
month = "12",
day = "1",
doi = "10.1007/978-1-59745-145-1_7",
language = "English (US)",
isbn = "9781588296252",
pages = "123--137",
booktitle = "Polyamine Cell Signaling",
publisher = "Humana Press",
address = "United States",

}

Shantz, L & Giordano, E 2006, Polyamine metabolism and the hypertrophic heart. in Polyamine Cell Signaling: Polyamine Cell Signaling. Humana Press, pp. 123-137. https://doi.org/10.1007/978-1-59745-145-1_7

Polyamine metabolism and the hypertrophic heart. / Shantz, Lisa; Giordano, Emanuele.

Polyamine Cell Signaling: Polyamine Cell Signaling. Humana Press, 2006. p. 123-137.

Research output: Chapter in Book/Report/Conference proceedingChapter

TY - CHAP

T1 - Polyamine metabolism and the hypertrophic heart

AU - Shantz, Lisa

AU - Giordano, Emanuele

PY - 2006/12/1

Y1 - 2006/12/1

N2 - Cardiac muscle hypertrophy is one of the most important compensatory responses of the heart to multiple stresses that may be placed on it. If the stress is not relieved, sustained hypertrophy may progress to dysfunction and heart failure. The polyamines putrescine, spermidine, and spermine increase within hours of various types of experimentally induced cardiac hypertrophy, along with ornithine decarboxylase (ODC) gene expression. Several animal models have implicated ODC induction as an important factor in the development of hypertrophy, particularly in response to β-adrenergic stimulation. Novel transgenic mouse lines that overexpress several enzymes of polyamine metabolism in the heart have been generated in recent years, and crosses of these lines have pointed to decarboxylated adenosylmethionine and its control by S-adenosylmethionine decarboxylase as another important element in maintaining cardiac polyamine homeostasis. The activity of arginase is thought to play a regulatory role in the biosynthesis of both nitric oxide (NO) and polyamines, and NO deficiency has been linked to the development of cardiac hypertrophy. Genetically altered mouse lines with changes in arginine and NO metabolism in the heart are available, many of which possess cardiac abnormalities. These models will provide a valuable means to address the interdependence of arginine and ornithine metabolism in the development of myocardial hypertrophy and failure. Use of these tools may lead to a better understanding of the control of the signaling pathways that include the polyamines, arginine, and NO, allowing future work to focus on the interactions between these pathways in the development of heart disease.

AB - Cardiac muscle hypertrophy is one of the most important compensatory responses of the heart to multiple stresses that may be placed on it. If the stress is not relieved, sustained hypertrophy may progress to dysfunction and heart failure. The polyamines putrescine, spermidine, and spermine increase within hours of various types of experimentally induced cardiac hypertrophy, along with ornithine decarboxylase (ODC) gene expression. Several animal models have implicated ODC induction as an important factor in the development of hypertrophy, particularly in response to β-adrenergic stimulation. Novel transgenic mouse lines that overexpress several enzymes of polyamine metabolism in the heart have been generated in recent years, and crosses of these lines have pointed to decarboxylated adenosylmethionine and its control by S-adenosylmethionine decarboxylase as another important element in maintaining cardiac polyamine homeostasis. The activity of arginase is thought to play a regulatory role in the biosynthesis of both nitric oxide (NO) and polyamines, and NO deficiency has been linked to the development of cardiac hypertrophy. Genetically altered mouse lines with changes in arginine and NO metabolism in the heart are available, many of which possess cardiac abnormalities. These models will provide a valuable means to address the interdependence of arginine and ornithine metabolism in the development of myocardial hypertrophy and failure. Use of these tools may lead to a better understanding of the control of the signaling pathways that include the polyamines, arginine, and NO, allowing future work to focus on the interactions between these pathways in the development of heart disease.

UR - http://www.scopus.com/inward/record.url?scp=84900097561&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84900097561&partnerID=8YFLogxK

U2 - 10.1007/978-1-59745-145-1_7

DO - 10.1007/978-1-59745-145-1_7

M3 - Chapter

SN - 9781588296252

SP - 123

EP - 137

BT - Polyamine Cell Signaling

PB - Humana Press

ER -

Shantz L, Giordano E. Polyamine metabolism and the hypertrophic heart. In Polyamine Cell Signaling: Polyamine Cell Signaling. Humana Press. 2006. p. 123-137 https://doi.org/10.1007/978-1-59745-145-1_7