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Despite mechanistic diversity, most strategies are constrained by a “cold” TME characterized by sparse TIL, abundant immunosuppressive mediators, and a restrictive BBB

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OxLDL components and their interaction with toll-like receptors (TLRs) 2 and 4, CD36 and other cellular receptors further mediate thromboinflammation enhancing tissue and organ damage culminating in organ failure, i.e., myocardial infarction, stroke, and pulmonary artery embolism ( FIGURE 7 The strong role of severe oxidative stress, reduced antioxidant defenses like GSH with increased lipid peroxidation and malondialdehyde generation ( via its incorporation into selenoproteins as the amino acid selenocysteine ( Administration of GSH precursors like cysteine/N-acetylcysteine, glycine and/or glutamic acid will facilitate the synthesis of GSH within each cell of the body including the atherosclerotic plaque, reducing ROS and LDL oxidation, enhancing NO production, and mitigating atherosclerosis and its complications ( Nuclear factor erythroid 2-related factor 2 plays a fundamental role in the response to oxidative stress and xenobiotic metabolism and detoxification, and the Nrf2 signaling pathway is intimately associated with development of atherosclerosis