Related Experiment Video

Updated: May 2, 2026

Production and Detection of Reactive Oxygen Species ROS in Cancers
07:17

Production and Detection of Reactive Oxygen Species ROS in Cancers

Published on: November 21, 2011

69.8K

Reactive oxygen species in diabetic nephropathy: friend or foe?

Tzvetanka Bondeva1, Gunter Wolf1

  • 1Department of Internal Medicine III, University Hospital Jena, Jena D-07740, Germany.

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association
|March 5, 2014
PubMed

Insights

Reactive oxygen species (ROS) are implicated in diabetes complications. New research questions the traditional focus on superoxide anion, suggesting a different target for treating diabetic nephropathy.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Endocrinology

Background:

  • Reactive oxygen species (ROS) act as signaling molecules in pathways like apoptosis, proliferation, damage, and inflammation.
  • Adverse ROS effects are linked to type 1 and type 2 diabetes mellitus onset and progression, including vascular, cardiac, and neurodegenerative complications, diabetic retinopathy, and nephropathy.
  • Superoxide anion generation due to hyperglycemia was considered the primary cause of these complications, despite detection challenges.

Purpose of the Study:

  • To review the novel concept regarding the role of ROS in diabetic nephropathy.
  • To question the established understanding of ROS involvement in diabetes complications.
  • To explore new therapeutic targets beyond superoxide anion suppression.

Main Methods:

  • Review of cellular and animal studies.
  • Analysis of recent findings on superoxide detection in diabetes.
  • Focus on novel concepts in ROS signaling in diabetic nephropathy.

Main Results:

  • Established view links ROS, particularly superoxide anion, to diabetes complications.
  • Recent research challenges the sole focus on superoxide anion, suggesting a need for re-evaluation.
  • The complexity of superoxide anion detection in vivo complicates direct attribution of its role.

Conclusions:

  • The traditional approach to treating diabetes-related complications by suppressing ROS may need re-evaluation.
  • Novel insights into ROS detection suggest a different primary target for diabetic nephropathy.
  • Further research is needed to understand the nuanced role of ROS in diabetes and its complications.
Keywords:
AMPKROSdiabetic nephropathysuperoxide anion

More Related Videos

Quantification of Reactive Oxygen Species Using 2′,7′-Dichlorofluorescein Diacetate Probe and Flow-Cytometry in Müller Glial Cells14:25

Quantification of Reactive Oxygen Species Using 2′,7′-Dichlorofluorescein Diacetate Probe and Flow-Cytometry in Müller Glial Cells

Published on: May 13, 2022

6.2K
Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice10:31

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice

Published on: May 2, 2025

798

Related Concept Videos

Diabetic Nephropathy01:28

Diabetic Nephropathy

Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration...
32
Diabetic Retinopathy01:27

Diabetic Retinopathy

DefinitionDiabetic retinopathy is a microvascular complication of diabetes affecting the retinal blood vessels.Risk FactorsDiabetic retinopathy is present in almost all individuals with type 1 diabetes and more than 60% of those with type 2 diabetes after two decades of disease.The risk increases with poor glycemic control, hypertension, dyslipidemia, smoking, pregnancy, and puberty.Although cataracts and glaucoma are also more frequent in people with diabetes, retinopathy remains the leading...
55
Diabetic Neuropathy01:22

Diabetic Neuropathy

DefinitionDiabetic neuropathy is nerve damage caused by long-standing diabetes mellitus. It results directly from prolonged high blood sugar levels.PathophysiologyThe pathophysiology of diabetic neuropathy involves both metabolic and vascular disturbances triggered by chronic hyperglycemia.Metabolic injury: Elevated glucose levels activate the polyol pathway within nerve cells, leading to the accumulation of sorbitol and fructose. This increases oxidative stress, disrupts normal nerve...
59
Bioactivation and Tissue Toxicity01:25

Bioactivation and Tissue Toxicity

Bioactivation is a metabolic process that transforms less reactive substances into highly reactive metabolites, initiating tissue toxicity. This transformation can lead to various toxic effects, including carcinogenesis and teratogenesis. Reactive metabolites are classified into two main types: electrophiles and free radicals.Electrophiles are electron-deficient species and are produced primarily by the enzyme cytochrome P-450 during the metabolism of compounds containing carbon, nitrogen, or...
151
Diabetic Ketoacidosis ll: Pathophysiology01:22

Diabetic Ketoacidosis ll: Pathophysiology

Diabetic ketoacidosis (DKA) is a metabolic emergency characterized by hyperglycemia, ketonemia, and metabolic acidosis. It results from severe insulin deficiency and an excess of counterregulatory hormones, leading to uncontrolled lipolysis, ketogenesis, and widespread electrolyte and fluid disturbances.Pathophysiology The central event in DKA is a profound loss of insulin action. Without insulin, glucose uptake in insulin-dependent tissues is impaired, while hepatic glucose production...
30
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
28