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Oxidized phosphatidylcholine (OxPC) refers to a heterogeneous group of bioactive lipids generated through the enzymatic or non-enzymatic oxidation of polyunsaturated fatty acids in phosphatidylcholine molecules [1, 14]. These lipids are prominent components of oxidized low-density lipoprotein (oxLDL) and serve as damage-associated molecular patterns (DAMPs) that are recognized by the innate immune system via pattern recognition receptors such as CD36, TLR2, and TLR4 [7, 17]. In pathological states, OxPCs accumulate at sites of inflammation and oxidative stress, where they promote leukocyte recruitment, cytokine production, and programmed cell death, including apoptosis and ferroptosis [3, 8, 18]. They play a critical role in the progression of chronic inflammatory diseases such as atherosclerosis, multiple sclerosis, and amyotrophic lateral sclerosis (ALS) [1, 5, 23]. Clinical assessment of OxPC levels, particularly those associated with apolipoprotein B, serves as a biomarker for cardiovascular risk and disease progression [6, 14]. Therapeutic approaches targeting OxPC involve the use of neutralizing monoclonal antibodies, such as E06, or small molecule analogs like VB-201 that inhibit OxPC-mediated signaling [7, 12, 15]. These interventions aim to mitigate the pro-inflammatory and cytotoxic effects of OxPCs while preserving the function of non-oxidized phospholipids [10, 12].
Neutralization of bioactive oxidized phospholipids and inhibition of TLR2/CD14-mediated signaling
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