Advanced lipid peroxidation end products in oxidative damage to proteins. Potential role in diseases and therapeutic prospects for the inhibitors

By A. Nègre-Salvayre, Christelle Coatrieux, C. Ingueneau, R. Salvayre. British Journal of Pharmacology, 2008

631 citations recorded by the source corpus.

Subfields: Biochemistry, Clinical Biochemistry, Endocrinology, Diabetes and Metabolism

View Paper: https://www.semanticscholar.org/paper/453e0b4b26a10ffd685976613ceb8cb38ffab9c0

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In Biochemistry

1. Liangyou Rui
2. G. Hotamışlıgil

In Endocrinology, Diabetes and Metabolism

1. Liangyou Rui
2. G. Hotamışlıgil

Citations in the corpus

• Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal (2014, background): “, crosslinking) by promoting intramolecular or intermolecular protein/DNA crosslinking that may induce profound alteration in the biochemical properties of biomolecules and accumulate during aging and in chronic diseases [72, 104, 182, 183].”
• Antioxidant Role for Lipid Droplets in a Stem Cell Niche of Drosophila (2015, neutral): “If hypoxia or other forms of oxidative stress induce ROS levels that are high enough to exceed cellular defense mechanisms, then they promote harmful oxidation and peroxidation chain reactions that can damage lipids, proteins, and nucleic acids (Negre-Salvayre et al., 2008).”
• ER Stress Sensor XBP1 Controls Anti-tumor Immunity by Disrupting Dendritic Cell Homeostasis (2015, background): “Other lipid peroxidation byproducts like acrolein, malondialdehyde, and 4-hydroxyhexenal form stable adducts with cellular proteins (Negre-Salvayre et al., 2008), suggesting that they might also induce immunosuppression in the tumor microenvironment by triggering ER stress in infiltrating innate…”
• Cellular and molecular mechanisms of renal fibrosis (2011, background): “Chronic hypoxia often coexists with increased oxidative stress and generation of ROS, which incites damage to biologically important macromolecules, including proteins, lipids and carbohydrates, and causes them to undergo structural modifications, leading to generation of advanced glycation end prod”
• Physiology and pathophysiology of carnosine. (2013, background): “A detailed description of the pathways of AGEs and ALEs formation is beyond the scope of the present review, but the reader is referred to some extensive reviews published on this aspect (11, 268, 285).”