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Treatment satisfaction and quality-of-life measures

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BPC-157's preclinical record in animal models is genuinely compelling the healing mechanisms proposed are biologically plausible and well-described [1]

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Key contributors to atherogenesis include oxidative stress (excess ROS oxidizing lipids and damaging endothelial cells), vascular inflammation (cytokine and chemokine release recruiting more immune cells), endothelial dysfunction (reduced NO bioavailability and loss of barrier integrity), and dyslipidemia (elevated LDL/triglycerides and low HDL)