Atherosclerosis: An intracellular deficiency in essential fatty acids

Cornwell, David G.; Panganamala, R.V.

doi:10.1016/0163-7827(81)90069-2

Cited by 40 publications

(14 citation statements)

References 115 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It was reported that UCP-1 expression in aortic smooth muscle cells produced hypertension, increased high fat diet-induced atherosclerosis without affecting cholesterol levels, enhanced superoxide anion production, and decreased the availability of nitric oxide, suggesting that mild respiratory uncoupling due to mitochondrial dysfunction causes atherosclerosis [164]. EFA deficiency promotes respiratory uncoupling [165][166][167] and atherosclerosis [117,168]. Atherosclerosis-free aortae have abundant amounts of EFA linoleate, whereas fatty streaks of early atherosclerosis are deficient in EFAs [169,170].…”

Section: Discussionmentioning

confidence: 99%

Essential Fatty Acids - A Review

Das¹

2006

CPB

348

208

View full text Add to dashboard Cite

Essential fatty acids (EFAs): cis-linoleic acid (LA) and alpha-linolenic acid (ALA) are essential for humans and their deficiency is rare in humans due to their easy availability in diet. EFAs are metabolized to their respective long-chain metabolites: dihomo-gamma-linolenic acid (DGLA), and arachidonic acid (AA) from LA; and eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) from ALA. Some of these long-chain metabolites form precursors to respective prostaglandins (PGs), thromboxanes (TXs), and leukotrienes (LTs), lipoxins (LXs) and resolvins. EFAs and their metabolites may function as endogenous angiotensin converting enzyme and HMG-CoA reductase inhibitors, nitric oxide enhancers, anti-hypertensives, and anti-atherosclerotic molecules. EFAs react with nitric oxide (NO) to yield respective nitroalkene derivatives that have cell-signaling actions via ligation and activation of peroxisome proliferator-activated receptors (PPARs). In several diseases such as obesity, hypertension, diabetes mellitus, coronary heart disease, alcoholism, schizophrenia, Alzheimer's disease, atherosclerosis, and cancer the metabolism of EFAs is altered. Thus, EFAs and their derivatives have significant clinical implications.

show abstract

Section: Discussionmentioning

confidence: 99%

Essential Fatty Acids - A Review

Das¹

2006

CPB

348

208

View full text Add to dashboard Cite

show abstract

“…- 63 We suggest that cell-cell contact between SMCs and recruited M0s participates in local and focal homeostatic control of fatty streak formation in the aorta through PGI 2 synthesis and that the disruption of this homeostatic control mechanism, possibly through a relative deficiency in A A, 67 is one of the many causes leading to the progression of atherosclerosis.…”

mentioning

confidence: 99%

“…Atherosclerotic lesions contain unusually high concentrations of 5,8,11-eicosatrienoic acid, which is a well-known characteristic of tissue AA deficiency, 65 and we have previously suggested that uncontrolled atherogenesis may be the result of a relative deficiency in SMC AA that would have as its effect diminished eicosanoid metabolism just when it was needed to regulate SMC proliferation. **- 67 An SMC AA deficiency would have a particularly significant effect when prostanoid synthesis involved in vascular homeostasis is localized by the functional effect of cell-cell contact between SMCs and M0s.…”

mentioning

confidence: 99%

Interactions between the monocyte/macrophage and the vascular smooth muscle cell. Stimulation of mitogenesis by a soluble factor and of prostanoid synthesis by cell-cell contact.

Zhang

Downs

Lindsey

et al. 1993

Arterioscler Thromb

View full text Add to dashboard Cite

The effect of soluble factors from the monocyte/macrophage (M0) on cell proliferation and the functional effects of cell-cell contact on the arachidonic acid (AA) cascade were studied with vascular smooth muscle cells (SMCs). Peripheral blood M0s were isolated by adherence or in a Percoll gradient, and alveolar M0s were obtained by lavage. Conditioned medium (CM) was prepared by preincubating M0s with medium alone or by separating SMC and M0 cocultures by a membrane insert Cell proliferation (image analysis) and 6-ketoprostaglandin F 1

show abstract

“…Studies performed by Cornwell et al [258,259] revealed that both -3 and -6 fatty acids (especially AA, EPA, and DHA) do inhibit smooth muscle cell proliferation and that this is related to the amount of lipid peroxides formed in the cells. These results have been confirmed by others [260,261].…”

Section: Effects On Endothelial Functionmentioning

confidence: 97%

“…Disease-free aortae have abundant concentrations of the essential fatty acid-linoleate, whereas fatty streaks (an early stage of atherosclerosis) are deficient in EFAs [153,157,158]. EFA deficiency promotes respiratory uncoupling [159,160] and atherosclerosis [1,161,162]. Bernal-Mizrachi et al showed that oxidative stress increases ROS generation and decreases NO formation and/or availability to be associated with smooth muscle expression of UCP-1.…”

Section: Uncoupling Protein-1 Essential Fatty Acids and Atherosclermentioning

confidence: 99%

Beneficial Actions of Polyunsaturated Fatty Acids in Cardiovascular Diseases: But, How and Why?

Das¹

2008

CNF

View full text Add to dashboard Cite

Omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), and to a limited extent -6 fatty acids: arachidonic acid (AA), -linolenic acid (GLA) and dihomo-GLA (DGLA), prevent cardiovascular disease, thrombosis and atherosclerosis, reduce cardiac arrhythmias, lower plasma cholesterol and triglycerides, lower high blood pressure and improve endothelial function. These beneficial actions of the fatty acids could be attributed to their ability to augment endothelial nitric oxide generation, inhibit HMG-CoA reductase and angiotensin converting enzyme (ACE) activities, block the production of pro-inflammatory cytokines, and modulate telomerase activity. AA, EPA, and DHA form precursors to anti-inflammatory molecules: lipoxins and resolvins that help in wound healing, inhibit the actions of pro-inflammatory eicosanoids, and suppress the production of free radicals and enhance nitric oxide (NO) generation. In addition, these fatty acids react with NO and NO-derived reactive nitrogen species to form nitroalkene derivative of fatty acids called as nitrolipids. Nitrolipids serve as potent ligands for peroxisome proliferator activated receptors (PPARs), inhibit platelet activation through elevation of cyclic AMP levels; suppress superoxide generation, degranulation, and integrin expression by human neutrophils, and induce vasorelaxation in a concentration dependent manner by releasing NO. Nitrolipids are formed at the sites of inflammation in significant amounts and increased by oxidative inflammatory reactions. Furthermore, -3 and -6 fatty acids interact with each other to enhance the formation of prostaglandin E 1 (PGE 1 ), prostacyclin (PGI 2 ), and PGI 3 , which are potent platelet anti-aggregators and vasodilators. Thus, GLA, DGLA, AA, EPA, and DHA when present in optimum amounts in the tissues, especially in endothelial cells, myocardium, platelets, and neutrophils, may aid in the prevention of cardiovascular diseases.

show abstract

Atherosclerosis: An intracellular deficiency in essential fatty acids

Cited by 40 publications

References 115 publications

Essential Fatty Acids - A Review

Essential Fatty Acids - A Review

Interactions between the monocyte/macrophage and the vascular smooth muscle cell. Stimulation of mitogenesis by a soluble factor and of prostanoid synthesis by cell-cell contact.

Beneficial Actions of Polyunsaturated Fatty Acids in Cardiovascular Diseases: But, How and Why?

Contact Info

Product

Resources

About