Yazar "Yaribeygi, Habib" seçeneğine göre listele

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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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    Hepatic effects of GLP-1 mimetics in diabetic milieu: A mechanistic review of involved pathways
    (Elsevier Science Inc, 2025) Yaribeygi, Habib; Kashian, Kiana; Moghaddam, Kimia Imani; Karim, Sheida Rashmeh; Bagheri, Narges; Karav, Sercan; Jamialahmadi, Tannaz
    Patients with diabetic are at a higher risk of developing hepatic disorders compared to non-diabetic individuals. This increased risk can be attributed to the diabetic environment, which triggers and exacerbates harmful pathways involved in both diabetic complications and hepatic disorders. Therefore, it is important to consider the use of antidiabetic agents that offer benefits beyond glycemic control and have positive effects on liver tissues. Glucagon-like peptide-1 (GLP-1) mimetics are a novel class of antidiabetic medications known for their potent blood sugar-lowering effects. Emerging evidence suggests that these drugs also have favorable effects on the liver. However, the precise effects and underlying mechanisms are not yet fully understood. In this review, we aim to provide a mechanistic perspective on the liver benefits of GLP-1 mimetics and outline the mediating mechanisms involved.
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    Neuroprotective and cognitive benefits of Semaglutide: Insights into the underlying molecular mechanisms
    (Pergamon-Elsevier Science Ltd, 2025) Yaghmayee, Shayan; Moazzeni, Atefeh Sadat; Jamialahmadi, Tannaz; Karav, Sercan; Yaribeygi, Habib; Kesharwani, Prashant; Sahebkar, Amirhossein
    Neuronal injury is a common complication in patients with diabetes. These injuries include a wide range of neurobehavioral complications that significantly reduce the neuronal network efficiency and quality of life in affected individuals. Currently, diabetes-induced neuronal complications are a major global health challenge, and many studies have been performed to prevent or slow their progression. Semaglutide is a novel form of glucagon-like peptide-1 (GLP-1) agonist agents that has recently been approved for diabetic patients to normalize glucose metabolism. However, some evidence indicates that it has extra-glycemic effects in some tissues as well as in the central nervous system. This evidence suggests that semaglutide can suppress some pathophysiological pathways involved in diabetes-induced neuronal complications and thus improve neuronal network efficiency. However, there is limited evidence to support all the pathways involved in mediating these benefits. In the current review, we aim to present the latest clinical and experimental findings on the possible benefits of semaglutide on major neuronal complications and to determine the possible molecular mechanisms involved.
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    Parkinson's disease and brain insulin signaling: Mechanisms and potential role of GLP-1 mimetics
    (Elsevier, 2025) Foroozanmehr, Behina; Hemmati, Mohammad Amin; Yaribeygi, Habib; Karav, Sercan; Jamialahmadi, Tannaz; Sahebkar, Amirhossein
    Parkinson's disease (PD) is a common neurodegenerative disorder characterized primarily by the degeneration of dopaminergic neurons in the substantia nigra pars compacta. The pathophysiology of PD is complex and multifactorial involving genetic factors, oxidative stress, mitochondrial dysfunction, impaired protein clearance, and neuroinflammation but recent evidence emphasizes the role of impaired brain insulin signaling. Insulin is a metabolic hormone with extensive effects on metabolic substrates but recent studies have demonstrated that it is also involved in central signaling pathways and induces different brain areas related to food craving, motor activities, cognitive abilities, and emotional feelings. Hence, it has been suggested that induction of brain insulin sensitivity may be a promising treatment for PD. Glucagon-like peptide-1 (GLP-1) mimetics are a new-generation class of antidiabetics that normalize glucose homeostasis via several pathways. Recent studies suggest extraglycemic benefits for GLP-1 mimetics against PD. GLP-1 mimetics can prevent or slow PD progression. Additionally, these agents can improve cognitive functions by improving brain insulin signaling pathways. In this review, we aim to highlight the role of brain insulin signaling in PD pathophysiology and discuss the possible benefits of GLP-1 mimetics in PD management.
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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.