Serotonin and pulmonary hypertension - from bench to bedside?

Margaret R MacLean, Yvonne Dempsie

Research output: Contribution to journalLiterature review

Abstract

The serotonin hypothesis of pulmonary arterial hypertension (PAH) arose owing to anorexigens, acting as indirect serotinergic agonists, causing PAH. However, it is now thought that serotonin plays an important role in the pathobiology of PAH per se. The rate-limiting enzyme in the synthesis of peripheral serotonin is tryptophan hydroxylase 1 (TPH1), serotonin can mediate pulmonary arterial smooth muscle cell proliferation via the serotonin transporter (SERT) and serotonin can induce pulmonary vasoconstriction via the 5-HT1B receptor in man. There is evidence that TPH1, SERT and 5-HT1B expression/activity can be upregulated in clinical PAH. This review discusses recent evidence implicating serotonin in the development of experimental and clinical PAH and suggests potential therapeutic targets.
Original languageEnglish
Pages (from-to)281-286
Number of pages6
JournalCurrent Opinion in Pharmacology
Volume9
Issue number3
DOIs
Publication statusPublished - Jun 2009

Fingerprint

Pulmonary Hypertension
Serotonin
Tryptophan Hydroxylase
Serotonin Plasma Membrane Transport Proteins
Receptor, Serotonin, 5-HT1B
Lung
Vasoconstriction
Smooth Muscle Myocytes
Cell Proliferation
Enzymes

Keywords

  • serotonin
  • pulmonary hypertension
  • serotinergic agonists
  • tryptophan hydroxylase 1
  • therapeutic targets

Cite this

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title = "Serotonin and pulmonary hypertension - from bench to bedside?",
abstract = "The serotonin hypothesis of pulmonary arterial hypertension (PAH) arose owing to anorexigens, acting as indirect serotinergic agonists, causing PAH. However, it is now thought that serotonin plays an important role in the pathobiology of PAH per se. The rate-limiting enzyme in the synthesis of peripheral serotonin is tryptophan hydroxylase 1 (TPH1), serotonin can mediate pulmonary arterial smooth muscle cell proliferation via the serotonin transporter (SERT) and serotonin can induce pulmonary vasoconstriction via the 5-HT1B receptor in man. There is evidence that TPH1, SERT and 5-HT1B expression/activity can be upregulated in clinical PAH. This review discusses recent evidence implicating serotonin in the development of experimental and clinical PAH and suggests potential therapeutic targets.",
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Serotonin and pulmonary hypertension - from bench to bedside? / MacLean, Margaret R; Dempsie, Yvonne.

In: Current Opinion in Pharmacology, Vol. 9, No. 3, 06.2009, p. 281-286.

Research output: Contribution to journalLiterature review

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T1 - Serotonin and pulmonary hypertension - from bench to bedside?

AU - MacLean, Margaret R

AU - Dempsie, Yvonne

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N2 - The serotonin hypothesis of pulmonary arterial hypertension (PAH) arose owing to anorexigens, acting as indirect serotinergic agonists, causing PAH. However, it is now thought that serotonin plays an important role in the pathobiology of PAH per se. The rate-limiting enzyme in the synthesis of peripheral serotonin is tryptophan hydroxylase 1 (TPH1), serotonin can mediate pulmonary arterial smooth muscle cell proliferation via the serotonin transporter (SERT) and serotonin can induce pulmonary vasoconstriction via the 5-HT1B receptor in man. There is evidence that TPH1, SERT and 5-HT1B expression/activity can be upregulated in clinical PAH. This review discusses recent evidence implicating serotonin in the development of experimental and clinical PAH and suggests potential therapeutic targets.

AB - The serotonin hypothesis of pulmonary arterial hypertension (PAH) arose owing to anorexigens, acting as indirect serotinergic agonists, causing PAH. However, it is now thought that serotonin plays an important role in the pathobiology of PAH per se. The rate-limiting enzyme in the synthesis of peripheral serotonin is tryptophan hydroxylase 1 (TPH1), serotonin can mediate pulmonary arterial smooth muscle cell proliferation via the serotonin transporter (SERT) and serotonin can induce pulmonary vasoconstriction via the 5-HT1B receptor in man. There is evidence that TPH1, SERT and 5-HT1B expression/activity can be upregulated in clinical PAH. This review discusses recent evidence implicating serotonin in the development of experimental and clinical PAH and suggests potential therapeutic targets.

KW - serotonin

KW - pulmonary hypertension

KW - serotinergic agonists

KW - tryptophan hydroxylase 1

KW - therapeutic targets

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DO - 10.1016/j.coph.2009.02.005

M3 - Literature review

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JO - Current Opinion in Pharmacology

JF - Current Opinion in Pharmacology

SN - 1471-4892

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