1997
DOI: 10.1016/s0163-7827(97)00005-2
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Phospholipid metabolism in the mammalian heart

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Cited by 20 publications
(13 citation statements)
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“…16). The mechanism of incorporation is unclear, but is probably mediated by the acyl-CoA: lysophosphatidylcholine acyltransferase, which is part of the deacylationreacylation of phospholipids (15,23). There is no evidence for a receptor-mediated regulation of the acyltransferases.…”
Section: Incorporation Ofmentioning
confidence: 99%
See 1 more Smart Citation
“…16). The mechanism of incorporation is unclear, but is probably mediated by the acyl-CoA: lysophosphatidylcholine acyltransferase, which is part of the deacylationreacylation of phospholipids (15,23). There is no evidence for a receptor-mediated regulation of the acyltransferases.…”
Section: Incorporation Ofmentioning
confidence: 99%
“…PLA activation is part of the deacylation-reacylation cycle (15) and thereby is involved in the remodeling of membrane phospholipids, for example, during hypertrophic cell growth.…”
Section: Introductionmentioning
confidence: 99%
“…1 are key components of membrane structure, modulate membrane enzyme activity, and participate in signaling pathways (1)(2)(3). The composition and content of PPL are altered in physiologic and pathologic cellular processes (4 -6).…”
Section: Phospholipids (Ppl)mentioning
confidence: 99%
“…The major phosphodiester components in the mammalian heart are glycerophosphocholine (GPCho) and glycerophosphoethanolamine (GPEth) [34−37]. Phosphomonoesters (PME), such as phosphocholine (PCho) and phosphoethanolamine (PEth), are commonly regarded as phospholipid precursors, whereas PDEs are mainly formed as phospholipid breakdown products [27,37]. The formation and decomposition of PDEs are controlled by the activity of several enzymes, such as phospholipases, lysophospolipases or possibly phosphodiesterases [37].…”
Section: Discussionmentioning
confidence: 99%
“…Phosphomonoesters (PME), such as phosphocholine (PCho) and phosphoethanolamine (PEth), are commonly regarded as phospholipid precursors, whereas PDEs are mainly formed as phospholipid breakdown products [27,37]. The formation and decomposition of PDEs are controlled by the activity of several enzymes, such as phospholipases, lysophospolipases or possibly phosphodiesterases [37]. Several changes in enzyme activity were reported in hypertensive heart disease and heart hypertrophy, but the regulation mechanisms of the interacting enzymes and the resulting metabolic changes remain unclear [37−39].…”
Section: Discussionmentioning
confidence: 99%