Oxidative stress and lipotoxicity

Hauck, Amy K.; Bernlohr, David A.

doi:10.1194/jlr.r066597

Cited by 221 publications

(184 citation statements)

References 117 publications

(128 reference statements)

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“…in turn, hydroxyl radical causes the formation of looh. Finally, a variety of reactive lipid aldehydes (rla) such as malondialdehyde (Mda) and 4-hydroxynonenal (4-hne) are created, with the ability to modify proteins through protein carbonylation (113,114). normally phase i and phase ii enzymes would detoxify rla products, but in individuals exhibiting metabolic syndrome, rlas accumulate causing damage to cells and their membranes.…”

Section: Oxidative Stress Reactive Oxygen Species Lipid Peroxidationmentioning

confidence: 99%

Obesity ‑ a risk factor for increased COVID‑19 prevalence, severity and lethality (Review)

et al. 2020

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Section: Oxidative Stress Reactive Oxygen Species Lipid Peroxidationmentioning

confidence: 99%

Obesity ‑ a risk factor for increased COVID‑19 prevalence, severity and lethality (Review)

et al. 2020

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“…Oxidative stress is a major mediator of lipotoxicity [49]. Conventional wisdom holds that increased mitochondrial respiration leads to H 2 O 2 formation through the electron transport chain, resulting in cellular stress [50].…”

Section: Peroxisomal Dysfunction In Disease Developmentmentioning

confidence: 99%

Peroxisomal Dysfunction in Age-Related Diseases

Cipolla

Lodhi

2017

Trends in Endocrinology & Metabolism

135

119

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Peroxisomes carry out many key functions related to lipid and reactive oxygen species (ROS) metabolism. The fundamental importance of peroxisomes for health in humans is underscored by the existence of devastating genetic disorders caused by impaired peroxisomal function or lack of peroxisomes. Emerging studies suggest that peroxisomal function may also be altered with aging and contribute to the pathogenesis of a variety of diseases, including diabetes and its related complications, neurodegenerative disorders, and cancer. With increasing evidence connecting peroxisomal dysfunction to the pathogenesis of these acquired diseases, the possibility of targeting peroxisomal function in disease prevention or treatment becomes intriguing. Here, we review recent developments in understanding the pathophysiological implications of peroxisomal dysfunctions outside the context of inherited peroxisomal disorders.

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“…The presence of high concentrations of intracellular free fatty acids can lead to oxidative stress caused by lipid peroxidation (Hauck and Bernlohr, 2016). In keeping with this, we found elevated levels of cellular reactive oxygen species (ROS) and lipid peroxidationderived protein modifications in B cells from the peritoneum compared with the spleen, and a relative increase in these parameters in the peritoneal B1a compared with B2 populations ( Figure 3E-F), suggesting that the peritoneal microenvironment inherently induces oxidative stress in association with lipid flux.…”

Section: B1 B Cells Take Up Exogenous Lipids and Undergo Cell Death Imentioning

confidence: 99%

B1a B cells require autophagy for metabolic homeostasis and self-renewal

Clarke

Riffelmacher

Braas³

et al. 2017

Preprint

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Specific metabolic programs are activated by immune cells to fulfil their functional roles, which include adaptations to their microenvironment. B1 B cells are tissue-resident, innatelike B cells. They have many distinct properties, such as the capacity to self-renew and the ability to rapidly respond to a limited repertoire of epitopes. The metabolic pathways that support these functions are unknown. We show that B1 B cells are bioenergetically more active than B2 B cells, with higher rates of glycolysis and oxidative phosphorylation, and depend on glycolysis. They acquire exogenous fatty acids, and store lipids in droplet form. Autophagy is differentially activated in B1a B cells, and deletion of the autophagy gene Atg7 leads to a selective loss of B1a B cells due to a failure of self-renewal. Autophagy-deficient B1a B cells downregulate critical metabolic genes and accumulate dysfunctional mitochondria. B1 B cells therefore, have evolved a distinct metabolism adapted to their residence and specific functional properties.

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Oxidative stress and lipotoxicity

Cited by 221 publications

References 117 publications

Obesity ‑ a risk factor for increased COVID‑19 prevalence, severity and lethality (Review)

Obesity ‑ a risk factor for increased COVID‑19 prevalence, severity and lethality (Review)

Peroxisomal Dysfunction in Age-Related Diseases

B1a B cells require autophagy for metabolic homeostasis and self-renewal

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