Peroxisomal hydrogen peroxide signaling: A new chapter in intracellular communication research

Fransen, Marc; Lismont, Celien

doi:10.1016/j.cbpa.2024.102426

Cited by 4 publications

(1 citation statement)

References 51 publications

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“…Cells deploy a array of antioxidant enzyme systems to regulate ROS, including SOD, which converts O 2− into H 2 O 2 . Furthermore, a group of enzymes is involved in the transformation of H 2 O 2 into water, including catalase (CAT), peroxiredoxin (PRDX), and glutathione peroxidase (GPX) ( Rhee, 2016 ; Nguyen et al, 2020 ; Fransen and Lismont, 2024 ), PRDX is a fundamental element of the cell’s antioxidative protective machinery, notable for its high attraction to H 2 O 2 and its widespread distribution throughout different cellular compartments. After oxidation, PRDX is regenerated by thioredoxin (TRX), which is in turn restored by thioredoxin reductase (TRXR) with the help of NADPH as an electron donor ( Gebicka and Krych-Madej, 2019 ).…”

Section: Sources and Control Of Reactive Oxygen Speciesmentioning

confidence: 99%

Research progress in mechanism of anticancer action of shikonin targeting reactive oxygen species

Qi,

Li,

et al. 2024

Front. Pharmacol.

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Excessive buildup of highly reactive molecules can occur due to the generation and dysregulation of reactive oxygen species (ROS) and their associated signaling pathways. ROS have a dual function in cancer development, either leading to DNA mutations that promote the growth and dissemination of cancer cells, or triggering the death of cancer cells. Cancer cells strategically balance their fate by modulating ROS levels, activating pro-cancer signaling pathways, and suppressing antioxidant defenses. Consequently, targeting ROS has emerged as a promising strategy in cancer therapy. Shikonin and its derivatives, along with related drug carriers, can impact several signaling pathways by targeting components involved with oxidative stress to induce processes such as apoptosis, necroptosis, cell cycle arrest, autophagy, as well as modulation of ferroptosis. Moreover, they can increase the responsiveness of drug-resistant cells to chemotherapy drugs, based on the specific characteristics of ROS, as well as the kind and stage of cancer. This research explores the pro-cancer and anti-cancer impacts of ROS, summarize the mechanisms and research achievements of shikonin-targeted ROS in anti-cancer effects and provide suggestions for designing further anti-tumor experiments and undertaking further experimental and practical research.

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Section: Sources and Control Of Reactive Oxygen Speciesmentioning

confidence: 99%

Research progress in mechanism of anticancer action of shikonin targeting reactive oxygen species

Qi,

Li,

et al. 2024

Front. Pharmacol.

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ROS-mediated regulation of β2AR function: Does oxidation play a meaningful role towards β2-agonist tachyphylaxis in airway obstructive diseases?

Teyani,

Moghaddam,

Moniri

2024

Biochemical Pharmacology

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Geographic characterization of RPE structure and lipid changes in the PEX1-p.Gly844Asp mouse model for Zellweger spectrum disorder

Omri,

Argyriou,

Pryce

et al. 2024

Preprint

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Peroxisome Biogenesis Disorders-Zellweger Spectrum (PBD-ZSD) are a heterogenous group of autosomal recessive disorders caused by defects inPEXgenes whose proteins are required for peroxisome assembly and function. Peroxisomes are ubiquitous organelles that play a critical role in complex lipid metabolism. Dysfunctional peroxisomes in ZSD cause multisystem effects, with progressive retinal degeneration (RD) leading to childhood blindness being one of the most frequent clinical findings. Despite progress in understanding the role of peroxisomes in normal cellular functions, much remains unknown about how their deficiency causes RD, and there is no treatment. To study RD pathophysiology in this disease, we used the knock-in PEX1-p.GlyG844Asp (G844D) mouse model of milder ZSD, which represents the common human PEX1-p.Gly843Asp allele. We previously reported diminished retinal function, functional vision, and neural retina structural defects in this model. Beyond the neural retina, structural defects in retinal pigment epithelium (RPE) have been reported in ZSD patients and murine models with single peroxisome enzyme deficiency, suggesting that RPE degeneration may contribute to overall RD progression in this disease. Here, we investigate the RPE phenotype in our PEX1-G844D mouse model, observing morphological, inflammatory, and lipid changes at 1, 3, and 6 months of age. We report that RPE cell degeneration appears at 3 months of age and worsens with time, starts in the dorsal pole, and is accompanied by subretinal inflammatory cell infiltration. We match these events with lipid remodelling using imaging mass spectrometry which allowed regional analysis specific to the RPE cell layer. We identified 47 lipid alterations that precede structural changes, 10 of which are localized to the dorsal pole. 32 of these lipid alterations persist to 3 months, with remodelling of the lipid signature at the dorsal pole. 14 new alterations occur concurrent with histological changes. Changes in peroxisome-dependent lipids detected by liquid chromatography tandem mass spectrometry (reduced docosahexanoic acid and increased very long chain lysophosphatidylcholines) are exacerbated over time. This study represents the first characterization of RPE in any animal model of ZSD, and the firstin situlipid analysis in any peroxisome-deficient tissue. Our findings reveal candidate lipid drivers that could be targeted to alleviate RD progression in ZSD, as well as candidate biomarkers that could be used to evaluate retinopathy progression and response to therapy.

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Peroxisomal hydrogen peroxide signaling: A new chapter in intracellular communication research

Cited by 4 publications

References 51 publications

Research progress in mechanism of anticancer action of shikonin targeting reactive oxygen species

Research progress in mechanism of anticancer action of shikonin targeting reactive oxygen species

ROS-mediated regulation of β2AR function: Does oxidation play a meaningful role towards β2-agonist tachyphylaxis in airway obstructive diseases?

Geographic characterization of RPE structure and lipid changes in the PEX1-p.Gly844Asp mouse model for Zellweger spectrum disorder

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