LOX‐1: Its cytotopographical variance and disease stress

Zeya, Bushra; Chandra, Nimai Chand

doi:10.1002/jbt.22375

Cited by 6 publications

(3 citation statements)

References 104 publications

(134 reference statements)

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“…As all statins can disrupt the binding of ox-LDL to the C-type lectin-like recognition domain of LOX-1, they all have the same effects of alleviating ox-LDL-induced endothelial ferroptosis (10). Previous studies have demonstrated that ox-LDL does not interact with xCT and GPx4 directly, but that it rather acts via LOX-1 (34)(35)(36). Similarly, all tested statins (atorvastatin, fluvastatin, lovastatin, pitavastatin and pravastatin) did not directly interact with xCT and GPx4 to improve ferroptosis (10), but protected endothelial cells from ferroptosis by disrupting the interaction of ox-LDL with LOX-1.…”

Section: Discussionmentioning

confidence: 99%

Novel function of fluvastatin in attenuating oxidized low‑density lipoprotein‑induced endothelial cell ferroptosis in a glutathione peroxidase4‑ and cystine‑glutamate antiporter‑dependent manner

Liu

Deng

et al. 2021

Exp Ther Med

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Oxidized low-density lipoprotein (ox-LDL) induces endothelial cell apoptosis and dysfunction. Statins are drugs that are clinically used to lower serum cholesterol levels, and they have been shown to exert vascular protective effects. In the present study, human umbilical vein endothelial cells were transfected with scramble control siRNA or siRNA specific for glutathione peroxidase (GPx)4 or cystine-glutamate antiporter (xCT). MTT, Matrigel and Transwell assays were used to evaluate cell proliferation, tube formation and migration, respectively. The levels of TNF-α, IL-α, 4-hydroxynonenal, GPx4 and xCT expression were detected by western blot analysis. It was demonstrated that ox-LDL promoted cytokine production and reduced the proliferation, migration and angiogenesis of endothelial cells. It was also observed that ox-LDL decreased GPx4 and xCT expression and induced ferroptosis. Furthermore, the inhibition of ferroptosis by deferoxamine mesylate attenuated ox-LDL-induced endothelial cell dysfunction and restored ox-LDL-decreased GPx4 and xCT expression. Consistent with these results, GPx4 and xCT knockdown by siRNA transfection aggravated ox-LDL-induced endothelial cell dysfunction and inhibition of proliferation. To the best of our knowledge, the present study was the first to discover that fluvastatin may protect endothelial cells from ox-LDL-induced ferroptosis and dysfunction. Furthermore, knockdown of GPx4 and xCT expression blunted the protective effects of fluvastatin on ox-LDL-treated endothelial cells. These data indicated a novel function of fluvastatin in the protection of endothelial cells from ox-LDL-induced ferroptosis, the mechanism of which involves the regulation of GPx4 and xCT.

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Section: Discussionmentioning

confidence: 99%

Novel function of fluvastatin in attenuating oxidized low‑density lipoprotein‑induced endothelial cell ferroptosis in a glutathione peroxidase4‑ and cystine‑glutamate antiporter‑dependent manner

Liu

Deng

et al. 2021

Exp Ther Med

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“…Additionally, VSMCs in individuals with T2D exhibit increased expression of the antiapoptotic protein Bcl-2, leading to resistance to cell death, enhanced proliferation, and a thicker media layer [ 110 ]. Prolonged exposure to elevated glucose levels induces oxidative stress in vascular cells, a crucial factor in the progression of atherosclerosis [ 111 , 112 , 113 , 114 ].…”

Section: Vascular Smooth Muscle Cell Phenotype Switching In Diseasementioning

confidence: 99%

Influence of DNA Methylation on Vascular Smooth Muscle Cell Phenotypic Switching

Yorn,

Kim,

Jeong

2024

IJMS

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Vascular smooth muscle cells (VSMCs) are crucial components of the arterial wall, controlling blood flow and pressure by contracting and relaxing the artery walls. VSMCs can switch from a contractile to a synthetic state, leading to increased proliferation and migratory potential. Epigenetic pathways, including DNA methylation, play a crucial role in regulating VSMC differentiation and phenotypic flexibility. DNA methylation involves attaching a methyl group to the 5’ carbon of a cytosine base, which regulates gene expression by interacting with transcription factors. Understanding the key factors influencing VSMC plasticity may help to identify new target molecules for the development of innovative drugs to treat various vascular diseases. This review focuses on DNA methylation pathways in VSMCs, summarizing mechanisms involved in controlling vascular remodeling, which can significantly enhance our understanding of related mechanisms and provide promising therapeutic approaches for complex and multifactorial diseases.

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“…Recent research has shown that gallic acid has anti-inflammatory effects and inhibits LOX-1 production [ 152 ]. Hydroxymethylglutaryl-CoA-reductase (HMG-CoA-reductase) inhibitors, namely, statins, reduce cardiovascular mortality by decreasing cholesterol as well as by non-lipid-related actions [ 153 ].…”

Section: Inhibition-strategies For Lox-1mentioning

confidence: 99%

Role of Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in inflammation and pathogen-associated interactions

Truthe,

Klassert,

Schmelz

et al. 2024

J Innate Immun

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Background: Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is known as a major receptor for oxidized low-density lipoproteins (oxLDL) and plays a significant role in the genesis of atherosclerosis. Recent research has shown its involvement in cancer, ischemic stroke, and diabetes. LOX-1 is a C-type lectin receptor and involved in the activation of immune cells and inflammatory processes. It may further interact with pathogens, suggesting a role in infections or the host's response. Summary: This review compiles the current knowledge of potential implications of LOX-1 in inflammatory processes and in host-pathogen interactions with a particular emphasis on its regulatory role in immune responses. Also discussed are genomic and structural variations found in LOX-1 homologues across different species as well as potential involvements of LOX-1 in inflammatory processes from the angle of different cell types and organ-specific interactions. Key messages: The results presented reveal both similar and different structures in human and murine LOX-1 and provide clues as to the possible origins of different modes of interaction. These descriptions raise concerns about the suitability, particularly of mouse models, that are often used in the analysis of its functionality in humans. Further research should also aim to better understand the mostly unknown binding and interaction mechanisms between LOX-1 and different pathogens. This pursuit will not only enhance our understanding of LOX-1 involvement in inflammatory processes, but also identify potential targets for immunomodulatory approaches.

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LOX‐1: Its cytotopographical variance and disease stress

Cited by 6 publications

References 104 publications

Novel function of fluvastatin in attenuating oxidized low‑density lipoprotein‑induced endothelial cell ferroptosis in a glutathione peroxidase4‑ and cystine‑glutamate antiporter‑dependent manner

Novel function of fluvastatin in attenuating oxidized low‑density lipoprotein‑induced endothelial cell ferroptosis in a glutathione peroxidase4‑ and cystine‑glutamate antiporter‑dependent manner

Influence of DNA Methylation on Vascular Smooth Muscle Cell Phenotypic Switching

Role of Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in inflammation and pathogen-associated interactions

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