Semaglutide, a recombinant DNA-derived long-acting GLP-1 receptor agonist, has emerged as a key player for patients with or without T2DM and obesity. It exerts pleiotropic effects by modulating glycemic regulation and energy homeostasis. Mechanistically, it stimulates glucose-dependent insulin secretion and suppresses glucagon while enhancing satiety through POMC/NPY modulation in the arcuate nucleus and delaying gastric emptying. Beyond its metabolic utility, semaglutide is cardioprotective, leveraging the PI3K/Akt and eNOS pathways to improve vasodilation, reduce reactive oxygen species (ROS), and stabilize atherosclerotic plaques by inhibiting pro-inflammatory cytokines like TNF-α. While it improves cardiac output via PKA-mediated inotropy, potential cardiotoxicity, including resting tachycardia and autonomic-driven arrhythmias, requires clinical vigilance, particularly regarding electrolyte imbalances in heart failure patients. Ultimately, its robust vasculoprotective profile reinforces its potential as a cornerstone in cardiovascular pharmacotherapy. Further research is needed to better understand the effects of semaglutide on cardiac function and pathologies as it advances as a cardiac drug. This review discusses multiple molecular targets of semaglutide on the heart.

Magnesium is an essential micronutrient that exerts fundamental roles at both the cellular and tissue levels, with broad therapeutic and preventive implications across a range of pathological conditions. Accumulating clinical and experimental evidence indicates that optimal magnesium homeostasis modulates key pathophysiological processes and serves as both a biological and prognostic marker in disorders such as stroke, myocardial infarction, type 2 diabetes mellitus, and renal failure. These disease states commonly originate from two major etiological determinants—hypertension and atherosclerosis—which share a unifying pro-inflammatory mediator: platelet-activating factor (PAF). PAF plays a central role in vascular inflammation by promoting platelet aggregation, macrophage infiltration, leukocyte adhesion, and vasomotor dysregulation. Importantly, magnesium demonstrates an inverse association with both platelet aggregation and PAF activity, underscoring its protective capacity in mitigating vascular inflammation and preserving endothelial function. The objective of this updated literature review is to elucidate the antagonistic interplay between magnesium and PAF, with a focus on its physiological and therapeutic significance across multiple organ systems. While emerging data support a modulatory role of magnesium in PAF-mediated inflammatory pathways, current evidence remains limited. Therefore, further mechanistic, pharmacological, and clinical investigations are warranted to clarify the multifaceted role of magnesium in attenuating PAF-driven disease processes.