The rise in the incidence of diabetes mellitus imposes great research and clinical efforts to decrease the prevalence and progression of this disease. Most of the therapeutic approaches used in clinical practice act in a repairing fashion to correct already developed pathologies or to slow their progression. A full understanding of the underlying mechanisms of diabetes etiology and pathogenesis is still needed for efficient and prompt intervention.
In that context, increased production of reactive oxygen species (ROS) has been recognized as a central event. Namely, oxidative stress is the connecting link between the main pathological hallmarks of diabetes (hyperglycemia, hyperlipidemia-related metabolic stress, and cytokines-related inflammatory stress) and consequent cellular damage and cell death. Decrease in the functional population of β-cells is the crucial process for triggering type 1 diabetes (T1D) and for the progression of type 2 diabetes (T2D). Also, cell death underlies the progression of diabetic complications that culminate in the injuries of many tissues and organs including liver, heart, retina, kidneys, and nervous system. So, the interference with redox-sensitive signaling pathways and cell death represents the promising approach for a decrease of the onset and improvement of the course of diabetes. To date, the involvement of various types of regulated cell death (apoptosis, necrosis, autophagy, and ferroptosis) in diabetes and diabetes-related pathologies has been demonstrated. Increased body of evidence strongly suggests that correction of ROS production and ROS-induced cell injury/death may be a powerful approach for the prevention and treatment of diabetes and diabetic complications. However, the success in clinical practice is still missing.
Within this Research Topic, we would like to welcome further investigations in this line. We hope to publish high-quality articles that will push progress in this field, and make direct or indirect connections to the clinical application and/or practice. We encourage the submission of original, mini-review, and review articles that:
· promote the understanding of underlying molecular mechanisms leading to cellular dysfunction and/or cell injury involved in the etiology, progression, and complications of T1D and T2D;
· characterize the type(s) of cell death involved in the removal of β-cells and of other cells affected in diabetes (e.g., endothelial cells, kidney mesangial cells, neurons, and neuroglia);
· investigate the possible approaches in the prevention and treatment of diabetes-related cell injuries/death;
· deal with the current challenges in the treatment of diabetes and diabetic complications.
This topic encourages, with no limitation, articles dealing with the redox aspects of the themes listed above.
The rise in the incidence of diabetes mellitus imposes great research and clinical efforts to decrease the prevalence and progression of this disease. Most of the therapeutic approaches used in clinical practice act in a repairing fashion to correct already developed pathologies or to slow their progression. A full understanding of the underlying mechanisms of diabetes etiology and pathogenesis is still needed for efficient and prompt intervention.
In that context, increased production of reactive oxygen species (ROS) has been recognized as a central event. Namely, oxidative stress is the connecting link between the main pathological hallmarks of diabetes (hyperglycemia, hyperlipidemia-related metabolic stress, and cytokines-related inflammatory stress) and consequent cellular damage and cell death. Decrease in the functional population of β-cells is the crucial process for triggering type 1 diabetes (T1D) and for the progression of type 2 diabetes (T2D). Also, cell death underlies the progression of diabetic complications that culminate in the injuries of many tissues and organs including liver, heart, retina, kidneys, and nervous system. So, the interference with redox-sensitive signaling pathways and cell death represents the promising approach for a decrease of the onset and improvement of the course of diabetes. To date, the involvement of various types of regulated cell death (apoptosis, necrosis, autophagy, and ferroptosis) in diabetes and diabetes-related pathologies has been demonstrated. Increased body of evidence strongly suggests that correction of ROS production and ROS-induced cell injury/death may be a powerful approach for the prevention and treatment of diabetes and diabetic complications. However, the success in clinical practice is still missing.
Within this Research Topic, we would like to welcome further investigations in this line. We hope to publish high-quality articles that will push progress in this field, and make direct or indirect connections to the clinical application and/or practice. We encourage the submission of original, mini-review, and review articles that:
· promote the understanding of underlying molecular mechanisms leading to cellular dysfunction and/or cell injury involved in the etiology, progression, and complications of T1D and T2D;
· characterize the type(s) of cell death involved in the removal of β-cells and of other cells affected in diabetes (e.g., endothelial cells, kidney mesangial cells, neurons, and neuroglia);
· investigate the possible approaches in the prevention and treatment of diabetes-related cell injuries/death;
· deal with the current challenges in the treatment of diabetes and diabetic complications.
This topic encourages, with no limitation, articles dealing with the redox aspects of the themes listed above.