Cellular death, reactive oxygen species (ROS) and diabetic complications

Cellular death, reactive oxygen species (ROS) and diabetic complications

2018 | Caroline Maria Oliveira Volpe, Pedro Henrique Villar-Delfino, Paula Martins Ferreira dos Anjos and José Augusto Nogueira-Machado
This review discusses the role of cellular death in diabetic complications, focusing on the signaling pathways triggered by hyperglycemia that lead to oxidative stress, advanced glycation end products (AGEs), and pro-inflammatory cytokine secretion. The review highlights the pivotal role of reactive oxygen species (ROS) and cellular death in these complications. It describes the signaling pathways involving diacylglycerol (DAG), protein kinase C (PKC), and NADPH-oxidase, which are activated by hyperglycemia and produce ROS. The review also explores the historical and recent advancements in drug development aimed at controlling these therapeutic targets. Key therapeutic targets discussed include DAG, PKC, and NADPH-oxidase, with a focus on their inhibitors. The review emphasizes the importance of downregulating ROS generation, oxidative stress, and cellular death to manage diabetic complications. It concludes by highlighting the need for further research to evaluate the effectiveness of these therapeutic targets in controlling diabetic complications.This review discusses the role of cellular death in diabetic complications, focusing on the signaling pathways triggered by hyperglycemia that lead to oxidative stress, advanced glycation end products (AGEs), and pro-inflammatory cytokine secretion. The review highlights the pivotal role of reactive oxygen species (ROS) and cellular death in these complications. It describes the signaling pathways involving diacylglycerol (DAG), protein kinase C (PKC), and NADPH-oxidase, which are activated by hyperglycemia and produce ROS. The review also explores the historical and recent advancements in drug development aimed at controlling these therapeutic targets. Key therapeutic targets discussed include DAG, PKC, and NADPH-oxidase, with a focus on their inhibitors. The review emphasizes the importance of downregulating ROS generation, oxidative stress, and cellular death to manage diabetic complications. It concludes by highlighting the need for further research to evaluate the effectiveness of these therapeutic targets in controlling diabetic complications.
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