Inflammation-related gene expression by lipid oxidation-derived products in the progression of atherosclerosis

Leonarduzzi, Gabriella; Gamba, Paola; Gargiulo, Simona; Biasi, Fiorella; Poli, Giuseppe

doi:10.1016/j.freeradbiomed.2011.09.031

Cited by 89 publications

(55 citation statements)

References 272 publications

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“…This is an important area of future investigation not only for possibly explaining the uptake of Lp(a) by SR-BI but also for explaining why Lp(a) may be more pro-atherogenic than LDL ( 30 ). The delivery of oxidized lipids to cells is believed to be pro-infl ammatory ( 32,33 ). Also of interest, CE In contrast, a marked delay in the plasma clearance of 3 H-CE-Lp(a) was evident in Sr-b1-KO mice compared with the control C57BL/6 mice.…”

Section: Sr-bi Mediates the Plasma Clearance Of Lp(a)mentioning

confidence: 99%

Scavenger receptor-BI is a receptor for lipoprotein(a)

Yang

Amar

Vaisman

et al. 2013

Journal of Lipid Research

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This article is available online at http://www.jlr.org Scavenger receptor class B type I (SR-BI) is a multi-ligand receptor. It binds a variety of oxidized as well as native lipoproteins, including high density lipoprotein (HDL) and low density lipoprotein (LDL) ( 1-4 ). SR-BI preferentially mediates the cellular uptake of neutral lipids over protein from lipoproteins by a process termed selective uptake. In the liver, the selective uptake of cholesteryl esters (CEs) from HDL potentiates the reverse cholesterol transport pathway, by increasing the hepatic excretion of cholesterol ( 5 ).Lipoprotein(a) [Lp(a)] is a pro-atherogenic lipoprotein particle that contains one copy of apolipoprotein(a) [apo(a)] covalently linked to apoB-100 by a disulfi de bond. It is found in some primates but is not present in most other mammalian species ( 6 ). Variation in the plasma level of Lp(a) is largely under genetic control, with polymorphisms in the kringle 4 repeat of apo(a) accounting for 40% of the variation ( 7 ). In general, apo(a) size is inversely associated with plasma Lp(a) level, but the relationship between apo(a) size and Lp(a) concentration varies among ethnic groups ( 8 ). In addition, a pentanucleotide repeat polymorphism in the 5 ′ control region of apo(a) accounts for 10-14% of the variation in Lp(a) concentrations in Caucasians ( 9 ).Human tracer studies have shown that plasma concentrations of Lp(a) were not only positively correlated with the secretion rates of Lp(a) protein, but also negatively correlated with the fractional catabolic rates (FCRs) of Lp(a) proteins, both apo(a) and apoB-100, indicating that plasma Lp(a) levels are also regulated by its rate of catabolism ( 10 ). However, the receptors that bind and mediate the catabolism of Lp Press, June 29, 2013 DOI 10.1194 Scavenger receptor-BI is a receptor for lipoprotein(a) Published, JLR Papers in

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Section: Sr-bi Mediates the Plasma Clearance Of Lp(a)mentioning

confidence: 99%

Scavenger receptor-BI is a receptor for lipoprotein(a)

Yang

Amar

Vaisman

et al. 2013

Journal of Lipid Research

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“…Secondary products of LPO (reactive carbonyl compounds), modify proteins and DNA bases (Poli et al, 2008). Therefore, LPO has been implicated as the underlying mechanisms in numerous disorders and diseases such as cardiovascular diseases, cancer, neurological disorders and aging (Leonarduzzi et al, 2012;Negre-Salvayre et al, 2010). Model studies have suggested possible beneficial effects of LPO products including antitumor and physiological signaling messenger (Niki, 2012).…”

Section: Lipid Peroxidationmentioning

confidence: 99%

Reactive oxygen species (ROS) generation, impacts on tissue oxidation and dietary management of non-communicable diseases: A review

Wafula¹,

Arnold²,

Calvin³

et al. 2017

Afr. J. Biochem. Res.

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Generation of reactive oxygen species (ROS) in biological systems has been reported to be a significant cause of inflammatory and metabolic diseases. More recently, ROS and in a particular ozone has also been implicated in the conversion of cholesterol to atherogenic compounds, secosterol A, and upon aldolization to secosterol-B. Secosterol-A is uniquely produced by cholesterol ozonolysis, while secosterol-B can also be generated through the reaction of cholesterol with singlet oxygen. On the other hand, lipid oxidation reactions generate hydroperoxides, which upon catalytic and/or enzymatic decomposition yields lipid peroxide products of significant importance to tissue health. The mechanism of formation of potent oxidants like ozone in biological systems has not been clearly demonstrated, with only a theory: That antibodies catalyze oxidation of water by singlet oxygen to yield a trioxidic species, like hydrogen trioxide, as an intermediate in hydrogen peroxide formation while a recent hypothesis indicates that ozone could also be an intermediate in the aforementioned pathway and could be generated from biological molecules in the presence of singlet oxygen. Similarly, there is new information being generated concerning the involvement of antioxidants and amino acids in either termination or propagation of oxidative processes in mammalian systems. This review explores mechanisms of ROS/ozone generation in tissues, lipid peroxidation, cholesterol oxidation and highlight dietary management of non-communicable diseases with a focus on the roles of antioxidants and amino acids.

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“…All these works give us valuable information about the proatherogenic effects mediated by OSEs. Several extensive reviews have summarised the main biological effects mediated by oxidised phospholipids on different cells involved in atherosclerosis [17,24,[27][28][29][30][31], the most important conclusions from them are next highlighted.…”

Section: Proatherogenic Signals Mediated By Pufa Peroxidation Productsmentioning

confidence: 99%

“…Others authors attribute anti-inflammatory effects to oxidized phospholipids because they abrogate the specific proinflammatory cascade activated by TLR2, TLR4, TLR3 and TLR9 [30]. Consequently, it is considered that oxidised phospholipids are non-canonical ligands for TLRs [24,29,37]. However, when CD36 recognises ox-LDL in association with TLRs, it activates NF-kB and induces the release of IL-1β [4,38].…”

Section: Proatherogenic Signals Mediated By Pufa Peroxidation Productsmentioning

confidence: 99%

Are oxidised low-density lipoproteins the true inducers of inflammation in atherosclerosis?

Montero-Vega¹

2014

Inflammasome

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Low-density lipoproteins become oxidised (ox-LDL) when retained in the arterial intima and are considered to be the inducers of inflammation in atherosclerosis. Peroxidation of phospholipids generates a variety of oxidised molecules in LDL and leads to the formation of oxidised lipid-protein adducts. These oxidative modifications are the target of various pattern recognition receptors (PRRs) and constitute immunogenic neoepitopes, termed oxidation-specific epitopes (OSEs). OSEs are thought to be a class of danger-associated molecular patterns (DAMPs) that mediate pro-inflammatory signals in atherosclerosis. Nevertheless, identical OSEs are generated on apoptotic cells that are identified by innate immunity through the same receptors to promote housekeeping tasks and immunosuppression. The present study provides an alternative point of view and proposes that OSEs are ‘waste-associated molecular patterns’ (WAMPs) recognised by innate immunity as a signal for the presence of oxidised waste that must be cleared without triggering inflammation. The hypothesis presented here states that ox-LDL are not inflammatory per se but instead polarise macrophages for housekeeping functions; however, other immune alerts, which are generated under the influence of risk factors, cooperate with them in switching macrophage polarisation towards dangerous phenotypes that complicate atheromas with different tendencies. This hypothesis of ‘immune cooperation’ explains why atheromas grow silently for decades and reveals atherosclerosis to be a dynamic disease that begins with the retention and oxidation of LDL in the arterial intima and ends with the formation of a thrombus, but in which the underlying immune process changes over time and differs between patients.

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Inflammation-related gene expression by lipid oxidation-derived products in the progression of atherosclerosis

Cited by 89 publications

References 272 publications

Scavenger receptor-BI is a receptor for lipoprotein(a)

Scavenger receptor-BI is a receptor for lipoprotein(a)

Reactive oxygen species (ROS) generation, impacts on tissue oxidation and dietary management of non-communicable diseases: A review

Are oxidised low-density lipoproteins the true inducers of inflammation in atherosclerosis?

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