Lipoproteins as targets and markers of lipoxidation

Afonso, Catarina; Spickett, Corinne M.

doi:10.1016/j.redox.2018.101066

Cited by 55 publications

(44 citation statements)

References 154 publications

(253 reference statements)

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“…HDLs have experimentally been shown to protect against LDL oxidation, thereby preventing the generation of proinflammatory oxidized lipids, mainly lipid hydroperoxides and short-chain oxidized phospholipids [36,[45][46][47]. The main antioxidant enzyme carried by HDL particles is paraoxonase 1 (PON1).…”

Section: Antioxidant and Anti-inflammatory Effectsmentioning

confidence: 99%

Advances in HDL: Much More than Lipid Transporters

Ben‐Aicha

Badimon

Vilahur

2020

IJMS

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High Density Lipoprotein (HDL) particles, beyond serving as lipid transporters and playing a key role in reverse cholesterol transport, carry a highly variable number of proteins, micro-RNAs, vitamins, and hormones, which endow them with the ability to mediate a plethora of cellular and molecular mechanisms that promote cardiovascular health. It is becoming increasingly evident, however, that the presence of cardiovascular risk factors and co-morbidities alters HDLs cargo and protective functions. This concept has led to the notion that metrics other than HDL-cholesterol levels, such as HDL functionality and composition, may better capture HDL cardiovascular protection. On the other hand, the potential of HDL as natural delivery carriers has also fostered the design of engineered HDL-mimetics aiming to improve HDL efficacy or as drug-delivery agents with therapeutic potential. In this paper, we first provide an overview of the molecules known to be transported by HDL particles and mainly discuss their functions in the cardiovascular system. Second, we describe the impact of cardiovascular risk factors and co-morbidities on HDL remodeling. Finally, we review the currently developed HDL-based approaches.

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Section: Antioxidant and Anti-inflammatory Effectsmentioning

confidence: 99%

Advances in HDL: Much More than Lipid Transporters

Ben‐Aicha

Badimon

Vilahur

2020

IJMS

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“…Lipid peroxidation could regulate hemostasis during pregnancy through at least two pathways. First, membrane lipids such as PS, which initiates and propagates both intrinsic and extrinsic coagulation, are highly sensitive to peroxidation [ 142 ]. Enzymatically oxidized phospholipids restore hemostasis in humans and mice with pathological bleeding, suggesting that lipid peroxidation enhances the procoagulant activity of these anionic phospholipids.…”

Section: Oxidative Stress In the Pe-induced Prothrombotic Statementioning

confidence: 99%

Oxidative Stress and Preeclampsia-Associated Prothrombotic State

et al. 2020

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Preeclampsia (PE) is a common obstetric disease characterized by hypertension, proteinuria, and multi-system dysfunction. It endangers both maternal and fetal health. Although hemostasis is critical for preventing bleeding complications during pregnancy, delivery, and post-partum, PE patients often develop a severe prothrombotic state, potentially resulting in life-threatening thrombosis and thromboembolism. The cause of this thrombotic complication is multi-factorial, involving endothelial cells, platelets, adhesive ligands, coagulation, and fibrinolysis. Increasing evidence has shown that hemostatic cells and factors undergo oxidative modifications during the systemic inflammation found in PE patients. However, it is largely unknown how these oxidative modifications of hemostasis contribute to development of the PE-associated prothrombotic state. This knowledge gap has significantly hindered the development of predictive markers, preventive measures, and therapeutic agents to protect women during pregnancy. Here we summarize reports in the literature regarding the effects of oxidative stress and antioxidants on systemic hemostasis, with emphasis on the condition of PE.

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“…Increased engagement of RAGE (Receptor for advanced glycation end products)/p38MAPK-NF-κB pathway may itself lead to increased production of C3 [80]. However, lipoxidation, the extent to which chronically elevated lipoproteins are oxidatively modified [81], is present and likely confounds identification of the trigger of complement activation [82]. In fact, in obese subjects, levels of C3a desArg/ASP and lipid hydroperoxide were significantly correlated [83].…”

Section: Discussionmentioning

confidence: 99%

Complement Properdin Regulates the Metabolo-Inflammatory Response to a High Fat Diet

et al. 2020

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Background and objectives: Overnutrition leads to a metabolic and inflammatory response that includes the activation of Complement. Properdin is the only amplifier of complement activation and increases the provision of complement activation products. Its absence has previously been shown to lead to increased obesity in mice on a high fat diet. The aim of this study was to determine ways in which properdin contributes to a less pronounced obese phenotype. Materials and Methods: Wild type (WT) and properdin deficient mice (KO) were fed a high-fat diet (HFD) for up to 12 weeks. Results: There was a significant increase in liver triglyceride content in the KO HFD group compared to WT on HFD. WT developed steatosis. KO had an additional inflammatory component (steatohepatitis). Analysis of AKT signalling by phosphorylation array supported a decrease in insulin sensitivity which was greater for KO than WT in liver and kidney. There was a significant decrease of C5L2 in the fat membranes of the KO HFD group compared to the WT HFD group. Circulating microparticles in KO HFD group showed lower presence of C5L2. Expression of the fatty acid transporter CD36 in adipose tissue was increased in KO on HFD and was also significantly increased in plasma of KO HFD mice compared to WT on HFD. CD36 was elevated on microparticles from KO on HFD. Ultrastructural changes consistent with obesity-associated glomerulopathy were observed for both HFD fed genotypes, but tubular strain was greater in KO. Conclusion: Our work demonstrates that complement properdin is a dominant factor in limiting the severity of obesity-associated conditions that impact on liver and kidney. The two receptors, C5L2 and CD36, are downstream of the activity exerted by properdin.

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Lipoproteins as targets and markers of lipoxidation

Cited by 55 publications

References 154 publications

Advances in HDL: Much More than Lipid Transporters

Advances in HDL: Much More than Lipid Transporters

Oxidative Stress and Preeclampsia-Associated Prothrombotic State

Complement Properdin Regulates the Metabolo-Inflammatory Response to a High Fat Diet

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