diabetic cardiomyopathies


Summary: Diabetes complications in which VENTRICULAR REMODELING in the absence of CORONARY ATHEROSCLEROSIS and hypertension results in cardiac dysfunctions, typically LEFT VENTRICULAR DYSFUNCTION. The changes also result in myocardial hypertrophy, myocardial necrosis and fibrosis, and collagen deposition due to impaired glucose tolerance.

Top Publications

  1. Levelt E, Gulsin G, Neubauer S, McCann G. MECHANISMS IN ENDOCRINOLOGY: Diabetic cardiomyopathy: pathophysiology and potential metabolic interventions state of the art review. Eur J Endocrinol. 2018;178:R127-R139 pubmed publisher
  2. Staels B. Cardiovascular Protection by Sodium Glucose Cotransporter 2 Inhibitors: Potential Mechanisms. Am J Cardiol. 2017;120:S28-S36 pubmed publisher
    ..This review discusses the main hypotheses suggested to date. ..
  3. Staels B. Cardiovascular Protection by Sodium Glucose Cotransporter 2 Inhibitors: Potential Mechanisms. Am J Med. 2017;130:S30-S39 pubmed publisher
    ..This review discusses the main hypotheses suggested to date. ..
  4. Pereira N, Novo Matos J, Baron Toaldo M, Bartoszuk U, Summerfield N, Riederer A, et al. Cats with diabetes mellitus have diastolic dysfunction in the absence of structural heart disease. Vet J. 2017;225:50-55 pubmed publisher
    ..The dysfunction seemed to progress rather than to normalize after 6 months, despite antidiabetic therapy. In cats with pre-existing heart disease, the development of DM could represent an important additional health risk. ..
  5. Jia C, Chen H, Wei M, Chen X, Zhang Y, Cao L, et al. Gold nanoparticle-based miR155 antagonist macrophage delivery restores the cardiac function in ovariectomized diabetic mouse model. Int J Nanomedicine. 2017;12:4963-4979 pubmed publisher
  6. Chung J, Park S, Cho D, Chung D, Chung M. Anemia, bilirubin, and cardiovascular autonomic neuropathy in patients with type 2 diabetes. Medicine (Baltimore). 2017;96:e6586 pubmed publisher
    ..In addition, our results suggest that the putative increased CAN risk associated with anemia might be mediated by a correlated decrease in serum bilirubin levels. ..
  7. Ma Z, Yuan Y, Xu S, Wei W, Xu C, Zhang X, et al. CTRP3 attenuates cardiac dysfunction, inflammation, oxidative stress and cell death in diabetic cardiomyopathy in rats. Diabetologia. 2017;60:1126-1137 pubmed publisher
    ..CTRP3 protected against DCM via activation of the AMPK? pathway. CTRP3 has therapeutic potential for the treatment of DCM. ..
  8. Zhang M, Wang S, Cheng Z, Xiong Z, Lv J, Yang Z, et al. Polydatin ameliorates diabetic cardiomyopathy via Sirt3 activation. Biochem Biophys Res Commun. 2017;493:1280-1287 pubmed publisher
    ..Our previous studies have shown that Polydatin (PD) alleviates cardiac dysfunction after myocardial infarction (MI) injury. Nevertheless, the mechanism by which PD regulates diabetic cardiomyopathy has not been reported...
  9. Yang F, Zhang L, Gao Z, Sun X, Yu M, Dong S, et al. Exogenous H2S Protects Against Diabetic Cardiomyopathy by Activating Autophagy via the AMPK/mTOR Pathway. Cell Physiol Biochem. 2017;43:1168-1187 pubmed publisher
    ..Our findings demonstrated that H2S decreases oxidative stress and protects against mitochondria injury, activates autophagy, and eventually leads to cardiac protection via the AMPK/mTOR pathway. ..

More Information


  1. Tasci I, Basgoz B, Saglam K. Glycemic control and the risk of microvascular complications in people with diabetes mellitus. Acta Diabetol. 2016;53:129-30 pubmed publisher
  2. Fuentes Antrás J, Picatoste B, Ramírez E, Egido J, Tunon J, Lorenzo O. Targeting metabolic disturbance in the diabetic heart. Cardiovasc Diabetol. 2015;14:17 pubmed publisher
  3. Zhang X, Pan L, Yang K, Fu Y, Liu Y, Chi J, et al. H3 Relaxin Protects Against Myocardial Injury in Experimental Diabetic Cardiomyopathy by Inhibiting Myocardial Apoptosis, Fibrosis and Inflammation. Cell Physiol Biochem. 2017;43:1311-1324 pubmed publisher
    ..This study is the first to demonstrate that H3 relaxin plays an anti-apoptotic, anti-fibrotic and anti-inflammatory role in DCM. ..
  4. Anjana R, Amutha A, Mohan V. Regularity of follow-up, glycemic burden, and risk of microvascular complications in patients with type 2 diabetes: a 9-year follow-up study : Reply to Dr. Tasci et al. Acta Diabetol. 2016;53:131-2 pubmed publisher
  5. Wu F, Wang B, Zhang S, Shi L, Wang Y, Xiong R, et al. FGF21 ameliorates diabetic cardiomyopathy by activating the AMPK-paraoxonase 1 signaling axis in mice. Clin Sci (Lond). 2017;131:1877-1893 pubmed publisher
    ..These findings suggest that FGF21 ameliorates DCM in part by activation of the AMPK-PON1 axis. ..
  6. Sun S, Yang S, Dai M, Jia X, Wang Q, Zhang Z, et al. The effect of Astragalus polysaccharides on attenuation of diabetic cardiomyopathy through inhibiting the extrinsic and intrinsic apoptotic pathways in high glucose -stimulated H9C2 cells. BMC Complement Altern Med. 2017;17:310 pubmed publisher
    ..APS decreases high glucose-induced H9C2 cell apoptosis by inhibiting the expression of pro-apoptotic proteins of both the extrinsic and intrinsic pathways and modulating the ratio of Bcl-2 to Bax in mitochondria. ..
  7. Pitt B, Zannad F. The detection of myocardial fibrosis: an opportunity to reduce cardiovascular risk in patients with diabetes mellitus?. Circ Cardiovasc Imaging. 2012;5:9-11 pubmed publisher
  8. Burchardt P, Zawada A, Wierusz Wysocka B. [Cardiovascular risk associated with abnormal metabolism of plasma lipoproteins in patients with diabetes mellitus]. Kardiol Pol. 2012;70:618-21 pubmed
  9. Carillion A, Feldman S, Na N, Biais M, Carpentier W, Birenbaum A, et al. Atorvastatin reduces ?-Adrenergic dysfunction in rats with diabetic cardiomyopathy. PLoS ONE. 2017;12:e0180103 pubmed publisher
    ..This effect is mediated by multiple modifications in expression of proteins in the ?-adrenergic signaling pathway, particularly through the NOS pathway. ..
  10. Li H, Bian Y, Zhang N, Guo J, Wang C, Lau W, et al. Intermedin protects against myocardial ischemia-reperfusion injury in diabetic rats. Cardiovasc Diabetol. 2013;12:91 pubmed publisher
    ..05 or p?<?0.01). By reducing oxidative stress, inflammation, and apoptosis, IMD may represent a promising novel therapeutic target mitigating diabetic ischemic heart injury. ..
  11. Bayeva M, Sawicki K, Ardehali H. Taking diabetes to heart--deregulation of myocardial lipid metabolism in diabetic cardiomyopathy. J Am Heart Assoc. 2013;2:e000433 pubmed publisher
  12. Frati G, Schirone L, Chimenti I, Yee D, Biondi Zoccai G, Volpe M, et al. An overview of the inflammatory signalling mechanisms in the myocardium underlying the development of diabetic cardiomyopathy. Cardiovasc Res. 2017;113:378-388 pubmed publisher
    ..This review article will provide an overview of the signalling molecular mechanisms linking diabetic cardiomyopathy to myocardial inflammation. ..
  13. Zhang Y, Sun X, Icli B, Feinberg M. Emerging Roles for MicroRNAs in Diabetic Microvascular Disease: Novel Targets for Therapy. Endocr Rev. 2017;38:145-168 pubmed publisher
  14. Vella R, Jackson D, Fenning A. ?9-Tetrahydrocannabinol Prevents Cardiovascular Dysfunction in STZ-Diabetic Wistar-Kyoto Rats. Biomed Res Int. 2017;2017:7974149 pubmed publisher
    ..Implications from this study suggest that cannabinoid receptors may be a potential new target for the treatment of diabetes-induced cardiovascular disease...
  15. Zheng J, Cheng J, Zhang Q, Xiao X. Novel insights into DNA methylation and its critical implications in diabetic vascular complications. Biosci Rep. 2017;37: pubmed publisher
    ..In this review, we will examine the growing role of DNA methylation in diabetes and its vascular complications, thus it can provide critical implications for the early prevention of diabetes and its vascular complications. ..
  16. de Paula D, Capuano V, Filho D, Carneiro A, de Oliveira Crema V, de Oliveira L, et al. Biological properties of cardiac mesenchymal stem cells in rats with diabetic cardiomyopathy. Life Sci. 2017;188:45-52 pubmed publisher
    ..The findings suggest, for the first time, that in chronic DM rats with overt DCM, cMSCs increase in number and exhibit changes in several functional properties, which could be implicated in the pathogenesis of diabetic cardiomyopathy. ..
  17. Ren J, Sowers J. Application of a novel curcumin analog in the management of diabetic cardiomyopathy. Diabetes. 2014;63:3166-8 pubmed publisher
  18. Yi F, Shang Y, Li B, Dai S, Wu W, Cheng L, et al. MicroRNA-193-5p modulates angiogenesis through IGF2 in type 2 diabetic cardiomyopathy. Biochem Biophys Res Commun. 2017;491:876-882 pubmed publisher
    ..MiR-193-5p is an active angiogenic factor in diabetic cardiomyopathy, possibly through inverse regulation on its downstream IGF2 gene. ..
  19. Geng H, Guan J. MiR-18a-5p inhibits endothelial-mesenchymal transition and cardiac fibrosis through the Notch2 pathway. Biochem Biophys Res Commun. 2017;491:329-336 pubmed publisher
    ..In conclusion, our findings demonstrated that miR-18a-5p/Notch2 signaling pathway participates in the regulation of high glucose-induced EndMT, and may act as a novel promising target for myocardial fibrosis in diabetic cardiomyopathy. ..
  20. Sukumaran V, Tsuchimochi H, Tatsumi E, Shirai M, Pearson J. Azilsartan ameliorates diabetic cardiomyopathy in young db/db mice through the modulation of ACE-2/ANG 1-7/Mas receptor cascade. Biochem Pharmacol. 2017;144:90-99 pubmed publisher
    ..Short-term treatment with AZL-3 reversed abnormal cardiac structural remodeling and partially improved glucose metabolism in db/db mice by modulating the ACE-2/ANG 1-7/Mas R pathway. ..
  21. Chen H, Yang X, Lu K, Lu C, Zhao Y, Zheng S, et al. Inhibition of high glucose-induced inflammation and fibrosis by a novel curcumin derivative prevents renal and heart injury in diabetic mice. Toxicol Lett. 2017;278:48-58 pubmed publisher
    ..The results of this study indicated that J17 can be potentially used as a cardio- and reno-protective agent and that targeting the P38 and AKT pathways may be an effective therapeutic strategy for diabetic complications. ..
  22. Liu P, Su J, Song X, Wang S. Activation of nuclear ?-catenin/c-Myc axis promotes oxidative stress injury in streptozotocin-induced diabetic cardiomyopathy. Biochem Biophys Res Commun. 2017;493:1573-1580 pubmed publisher
    ..The present study demonstrated that activated nuclear ?-catenin/c-Myc axis was responsible for oxidative cardiac impairment of DCM. Therefore, repressing functional nuclear ?-catenin may provide a hopeful therapeutic strategy for DCM...
  23. Zhang Y, Wu H, Lv F, Xiao R. MG53: Biological Function and Potential as a Therapeutic Target. Mol Pharmacol. 2017;92:211-218 pubmed publisher
    ..In this review, we comprehensively summarize current research progress on the biologic functions and therapeutic potential of MG53. ..
  24. Laakso M. Heart in diabetes: a microvascular disease. Diabetes Care. 2011;34 Suppl 2:S145-9 pubmed publisher
  25. Wu B, Lin J, Luo J, Han D, Fan M, Guo T, et al. Dihydromyricetin Protects against Diabetic Cardiomyopathy in Streptozotocin-Induced Diabetic Mice. Biomed Res Int. 2017;2017:3764370 pubmed publisher
    ..DHM may have a great therapeutic potential in the treatment of DCM. ..
  26. . Risk Factors for Cardiovascular Disease in Type 1 Diabetes. Diabetes. 2016;65:1370-9 pubmed publisher
    ..70 and 0.77, respectively, and for the final models, including all significant risk factors, were 0.75 and 0.82. Although many conventional CVD risk factors apply in T1DM, hyperglycemia is an important risk factor second only to age. ..
  27. Sahoo S, Emanueli C. Exosomes in Diabetic Cardiomyopathy: The Next-Generation Therapeutic Targets?. Diabetes. 2016;65:2829-31 pubmed publisher
  28. Lorenzo Almorós A, Tunon J, Orejas M, Cortes M, Egido J, Lorenzo O. Diagnostic approaches for diabetic cardiomyopathy. Cardiovasc Diabetol. 2017;16:28 pubmed publisher
    ..Thus, we suggest a combination of minimally-invasive diagnosis tools for human DCM recognition based on imaging techniques and measurements of related plasma biomarkers. ..
  29. Shaw J, Cooper M. Guidelines and their use in clinical practice. Diab Vasc Dis Res. 2014;11:3-4 pubmed publisher
  30. Lytvyn Y, Bjornstad P, Udell J, Lovshin J, Cherney D. Sodium Glucose Cotransporter-2 Inhibition in Heart Failure: Potential Mechanisms, Clinical Applications, and Summary of Clinical Trials. Circulation. 2017;136:1643-1658 pubmed publisher
    ..Finally, we provide a detailed overview and summary of ongoing cardiovascular outcome trials with SGLT2 inhibitors. ..
  31. Windecker S, Kolh P, Alfonso F, Collet J, Cremer J, Falk V, et al. 2014 ESC/EACTS Guidelines on myocardial revascularization: The Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS)Developed with the special contribut. Eur Heart J. 2014;35:2541-619 pubmed publisher
  32. Dei Cas A, Fonarow G, Gheorghiade M, Butler J. Concomitant diabetes mellitus and heart failure. Curr Probl Cardiol. 2015;40:7-43 pubmed publisher
  33. Xu Z, Tong Q, Zhang Z, Wang S, Zheng Y, Liu Q, et al. Inhibition of HDAC3 prevents diabetic cardiomyopathy in OVE26 mice via epigenetic regulation of DUSP5-ERK1/2 pathway. Clin Sci (Lond). 2017;131:1841-1857 pubmed publisher
    ..The present study indicates the potential application of HDAC3 inhibitor for the prevention of DCM. ..
  34. Singh G, Khanna S, Raut S, Sharma S, Sharma R, Khullar M. DUSP-1 gene expression is not regulated by promoter methylation in diabetes-associated cardiac hypertrophy. Ther Adv Cardiovasc Dis. 2017;11:147-154 pubmed publisher
    ..Methylation-mediated silencing of the DUSP-1 promoter does not appear to be associated with reduced expression, indicating the involvement of other factors in specific suppression of DUSP-1 in diabetes-associated cardiac hypertrophy. ..
  35. Watkins H, Ashrafian H, Redwood C. Inherited cardiomyopathies. N Engl J Med. 2011;364:1643-56 pubmed publisher
  36. Tate M, Grieve D, Ritchie R. Are targeted therapies for diabetic cardiomyopathy on the horizon?. Clin Sci (Lond). 2017;131:897-915 pubmed publisher
  37. Prakoso D, De Blasio M, Qin C, Rosli S, Kiriazis H, Qian H, et al. Phosphoinositide 3-kinase (p110?) gene delivery limits diabetes-induced cardiac NADPH oxidase and cardiomyopathy in a mouse model with established diastolic dysfunction. Clin Sci (Lond). 2017;131:1345-1360 pubmed publisher
  38. Zhang M, Zhao Y, Ma W, Xu J, Wang J, Chen M, et al. [Therapeutic effect of combined use of FGF1-loaded nano-liposomes and ultrasound-targeted microbubble destruction technique on treating rats with experimental diabetic cardiomyopathy]. Zhonghua Xin Xue Guan Bing Za Zhi. 2017;45:427-433 pubmed publisher
    ..05)?fgf1????fgf1???????fgf1??????utmd????????????????dcm?(p?<0.05)??fgf1??????utmd?????????????????fgf1????fgf1??????(p?<0.05)? ??? fgf1???????utmd?????dcm?????????????????dcm???????. ..
  39. Rawal S, Ram T, Coffey S, Williams M, Saxena P, Bunton R, et al. Differential expression pattern of cardiovascular microRNAs in the human type-2 diabetic heart with normal ejection fraction. Int J Cardiol. 2016;202:40-3 pubmed publisher
  40. Zhao C, Zhang Y, Liu H, Li P, Zhang H, Cheng G. Fortunellin protects against high fructose-induced diabetic heart injury in mice by suppressing inflammation and oxidative stress via AMPK/Nrf-2 pathway regulation. Biochem Biophys Res Commun. 2017;490:552-559 pubmed publisher
    ..For the first time, our study suggested that Fortunellin protected against fructose-induced inflammation and oxidative stress by enhancing AMPK/Nrf2 pathway in diabetic mice and cardiomyocytes with fructose treatment. ..