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Mechanistic gaps in pathway crosstalk and causality: Current studies have primarily focused on individual pathways (e.g., Nrf2-mediated antioxidant defense and TGF-/SmadHDAC3-driven fibrosis) but lack insights into the core molecular hubs integrating these networks

Further studies with a larger cohort are necessary

This means that GLP-1 receptor agonists can limit and stabilize the development of atherosclerotic plaques through anti-inflammatory mechanisms and by preventing vascular remodeling, which ultimately can provide protective effects against major adverse cardiac events (MACEs)

This mistake leads to bacterial contamination and wasted peptides

The pleiotropic functions of reactive oxygen species in cancer