Oxidative stress signaling pathways and reactive oxygen species accumulation play a major role in the pathogenesis of diabetic cardiomyopathy, representing potential targets for future therapies.
This review highlights oxidative stress signaling pathways as a key pathophysiological mechanism and potential therapeutic target in the management of diabetic cardiomyopathy.
As a serious cardiovascular complication, diabetic cardiomyopathy (DCM) refers to diabetes-related changes in myocardial structure and function, which is obviously different from those cardiomyopathy secondary to hypertension, coronary heart disease, and valvular disease. The clinical features of DCM are left ventricular hypertrophy, myocardial fibrosis, and impaired diastolic function. DCM will lead to cardiac dysfunction, eventually progress to cardiac arrhythmia, heart failure, and sudden cardiac death. At present, the pathogenesis of DCM is complex and not fully elucidated, and oxidative stress (OS), inflammatory response, glucolipid metabolism disorder, etc., are considered as the potential pathophysiological mechanisms. As a consequence, there is no specific and effective treatment for DCM. OS refers to the imbalance between reactive oxygen species (ROS) accumulation and scavenging, oxidation, and antioxidants in vivo, which is widely studied in DCM. Numerous studies have pointed out that regulating the OS signaling pathways and reducing the generation and accumulation of ROS are potential directions for the treatment of DCM. This review summarizes the major OS signaling pathways that are related to the pathogenesis of DCM, providing ideas about further research and therapy.
Tang et al. (Sat,) conducted a review in Diabetic cardiomyopathy. Oxidative stress signaling pathways was evaluated. Oxidative stress signaling pathways and reactive oxygen species accumulation play a major role in the pathogenesis of diabetic cardiomyopathy, representing potential targets for future therapies.