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Current Molecular Pharmacology

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Mini-Review Article

Therapeutic Potential of Resveratrol in Diabetic Nephropathy According to Molecular Signaling

Author(s): Marziyeh Salami, Raziyeh Salami, Alireza Mafi, Mohammad-Hossein Aarabi, Omid Vakili and Zatollah Asemi*

Volume 15, Issue 5, 2022

Published on: 01 March, 2022

Article ID: e171221199120 Pages: 20

DOI: 10.2174/1874467215666211217122523

Price: $65

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Abstract

Background: Diabetic nephropathy (DN), as a severe complication of diabetes mellitus (DM), is a crucial menace for human health and survival and remarkably elevates the healthcare systems’ costs. Therefore, it is worth noting to identify novel preventive and therapeutic strategies to alleviate the disease conditions. Resveratrol, as a well-defined anti-diabetic/ antioxidant agent has capabilities to counteract diabetic complications. It has been predicted that resveratrol will be a fantastic natural polyphenol for diabetes therapy in the next few years.

Objective: Accordingly, the current review aims to depict the role of resveratrol in the regulation of different signaling pathways that are involved in the reactive oxygen species (ROS) production, inflammatory processes, autophagy, and mitochondrial dysfunction, as critical contributors to DN pathophysiology.

Results: The pathogenesis of DN can be multifactorial; hyperglycemia is one of the prominent risk factors of DN development that is closely related to oxidative stress. Resveratrol, as a well-defined polyphenol, has various biological and medicinal properties, including anti-diabetic, anti-inflammatory, and anti-oxidative effects.

Conclusion: Resveratrol prevents kidney damages that are caused by oxidative stress, enhances antioxidant capacity, and attenuates the inflammatory and fibrotic responses. For this reason, resveratrol is considered an interesting target in DN research due to its therapeutic possibilities during diabetic disorders and renal protection.

Keywords: Diabetic nephropathy, resveratrol, signaling pathway, oxidative stress, inflammation, cellular mechanisms.

Graphical Abstract

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