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    Exploring the antioxidant properties of semaglutide: A comprehensive review
    (Elsevier Science Inc, 2024) Yaribeygi, Habib; Maleki, Mina; Forouzanmehr, Behina; Kesharwani, Prashant; Jamialahmadi, Tannaz; Karav, Sercan; Sahebkar, Amirhossein
    Patients with diabetes commonly experience an aberrant production of free radicals and weakened antioxidative defenses, making them highly susceptible to oxidative stress development. This, in turn, can induce and promote diabetic complications. Therefore, utilizing antidiabetic agents with antioxidative properties can offer dual benefits by addressing hyperglycemia and reducing oxidative damage. Semaglutide, a recently approved oral form of glucagon-like peptide-1 (GLP-1) analogues, has shown potent antidiabetic effects. Additionally, recent studies have suggested that it possesses antioxidative properties. However, the exact effects and the molecular pathways involved are not well understood. In this review, we present the latest findings on the antioxidative impacts of semaglutide and draw conclusions about the mechanisms involved.
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    The Emerging role of lipoprotein(a) in diabetic kidney disease: possible pathophysiological links and unresolved mechanisms
    (Elsevier Ireland Ltd, 2026) Yaribeygi, Habib; Maleki, Mina; Karav, Sercan; Kesharwani, Prashant; Sahebkar, Amirhossein
    Diabetic kidney disease (DKD) is one of the most serious microvascular complications of diabetes mellitus and a leading cause of end-stage renal disease worldwide. Although hyperglycemia and hypertension are well-established drivers of DKD, accumulating evidence suggests that additional factors, such as lipoprotein(a) [Lp (a)], may contribute to its pathogenesis. Lp(a) is a genetically determined lipoprotein with pro-atherogenic, proinflammatory, and pro-thrombotic properties, and elevated circulating levels have been associated with increased cardiovascular and renal risk in diabetic individuals. In this review, we summarize the current understanding of the relationship between Lp(a) and DKD, with a focus on the proposed molecular mechanisms. These include activation of TGF-beta/Smad signaling leading to fibrosis, induction of oxidative stress, chronic inflammation, endothelial dysfunction, impaired fibrinolysis, and direct injury to podocytes resulting in proteinuria. While several clinical and experimental studies support the involvement of Lp(a) in these pathways, the precise molecular mediators remain largely undefined. Understanding these mechanisms may offer novel insights into the pathophysiology of DKD and identify new therapeutic targets. This article aims to provide a comprehensive overview of the potential role of Lp(a) in DKD and to highlight areas requiring further investigation.