Pathophysiological Fundamentals of Diabetic Cardiomyopathy.
Diabetic cardiomyopathy (DCM) was first recognized more than four decades ago and occurred independent of cardiovascular diseases or hypertension in both type 1 and type 2 diabetic patients. The exact mechanisms underlying this disease remain incompletely understood. Several pathophysiological bases responsible for DCM have been proposed, including the presence of hyperglycemia, nonenzymatic glycosylation of large molecules (e.g., proteins), energy metabolic disturbance, mitochondrial damage and dysfunction, impaired calcium handling, reactive oxygen species formation, inflammation, cardiac cell death, and cardiac hypertrophy and fibrosis, leading to impairment of cardiac contractile functions. Increasing evidence also indicates the phenomenon called "metabolic memory" for diabetes-induced cardiovascular complications, for which epigenetic modulation seemed to play an important role, suggesting that the aforementioned pathogenic bases may be regulated by epigenetic modification. Therefore, this review aims at briefly summarizing the current understanding of the pathophysiological bases for DCM. Although how epigenetic mechanisms play a role remains incompletely understood now, extensive clinical and experimental studies have implicated its importance in regulating the cardiac responses to diabetes, which are believed to shed insight into understanding of the pathophysiological and epigenetic mechanisms for the development of DCM and its possible prevention and/or therapy. © 2017 American Physiological Society. Compr Physiol 7:693-711, 2017.
Center of Cardiovascular Diseases, the First Hospital of Jilin University, Changchun, China.|Pediatric Research Institute at the Department of Pediatrics of the University of Louisville, Louisville, Kentucky, USA.
Xinyue
X
Hu
Center of Cardiovascular Diseases, the First Hospital of Jilin University, Changchun, China.|Pediatric Research Institute at the Department of Pediatrics of the University of Louisville, Louisville, Kentucky, USA.
Tao
T
Bai
Center of Cardiovascular Diseases, the First Hospital of Jilin University, Changchun, China.|Pediatric Research Institute at the Department of Pediatrics of the University of Louisville, Louisville, Kentucky, USA.
Zheng
Z
Xu
Department of Hematological Disorders the First Hospital of Jilin University, Changchun, China.
Qiuju
Q
Liu
Center of Cardiovascular Diseases, the First Hospital of Jilin University, Changchun, China.
Yang
Y
Zheng
Pediatric Research Institute at the Department of Pediatrics of the University of Louisville, Louisville, Kentucky, USA.|Wendy Novak Diabetes Care Center, University of Louisville, Louisville, Kentucky, USA.
Lu
L
Cai
D000818:Animals; D017209:Apoptosis / Q000502:physiology; D006332:Cardiomegaly / Q000503:physiopathology; D019175:DNA Methylation / Q000502:physiology; D058065:Diabetic Cardiomyopathies / Q000235:genetics / Q000473:pathology / Q000503:physiopathology*; D044127:Epigenesis, Genetic / Q000502:physiology; D005109:Extracellular Matrix / Q000502:physiology; D005355:Fibrosis; D006801:Humans; D035683:MicroRNAs / Q000235:genetics; D009206:Myocardium / Q000473:pathology; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology
D035683:MicroRNAs