Molecular insights into diabetic cardiomyopathy

Authors

  • Chayanika Barman Department of Biochemistry, Maharishi Markandeshwar Institute of Medical Sciences and Research (MMIMSR), Mullana, Ambala, Haryana
  • Rajesh Pandey Department of Biochemistry, Maharishi Markandeshwar Institute of Medical Sciences and Research (MMIMSR), Mullana, Ambala, Haryana
  • Jasbir Singh Department of Biochemistry, Maharishi Markandeshwar Institute of Medical Sciences and Research (MMIMSR), Mullana, Ambala, Haryana
  • Kuldip S. Sodhi Department of Biochemistry, Maharishi Markandeshwar Institute of Medical Sciences and Research (MMIMSR), Mullana, Ambala, Haryana

DOI:

https://doi.org/10.18203/2320-6012.ijrms20150230

Keywords:

Diabetic cardiomyopathy, Insulin, Genes, Apoptosis, Fibrosis, Therapy

Abstract

Diabetes mellitus affects the heart in 3 ways: (1) coronary artery disease (CAD) due to accelerated atherosclerosis; (2) cardiac autonomic neuropathy (CAN); and (3) diabetic cardiomyopathy (DbCM). Although there is high awareness among clinicians about the first two entities, DbCM is poorly recognized by most physicians and diabetologists. DbCM, first described by Rubler et al. in 1972, is defined as myocardial dysfunction occurring in patients with diabetes in the absence of CAD, hypertension, or valvular heart disease. The development of DbCM is multi-factorial including autonomic dysfunction, metabolic derangements, abnormalities in ion homeostasis, alteration in structural proteins, and interstitial fibrosis. Chronic hyperglycemia is thought to play a central role in the development of DbCM. The main metabolic abnormalities in diabetes are hyperglycemia, hyperlipidemia and inflammation, all of which stimulate generation of reactive oxygen/nitrogen species which result in reduction of myocardial contractility and acceleration of fibrosis besides cellular DNA damage and cardiomyocyte apoptosis. In addition, advanced glycation end products (AGEs) indirectly exert their detrimental effect on the myocardium by interacting and up-regulating their receptors, including receptors of AGE and galectin-3. This results in activation of transcription factors, such as nuclear factor-kB (NF-kB). The NF-kB dependent genes, in turn, trigger several pathways that induce production of pro-inflammatory cytokines and cause myocardial damage. All these molecular events are potential therapeutic targets in DbCM.

 

References

Ren J, Sowers JR. Application of a novel curcumin analog in the management of diabetic cardiomyopathy. Diabetes. 2014;63:3166-8.

Battiprolu PK, Lopez-Crisosto C, Wang ZV, Nemchenko A, Lavandero S, Hill JA. Diabetic cardiomyopathy and metabolic remodeling of the heart. Life Sci. 2013;92:609-15.

Ojji DB (2011). Diabetic Cardiomyopathy. In: Zimerimg M, ed. Recent Advances in the Pathogenesis, Prevention and Management of Type 2 Diabetes and its Complications. Europe: InTech; 2011: 105-18. ISBN: 978-953-307-597-6. Available from: http://www.intechopen.com/books/recent-advances-in-the-pathogenesis-preventionand-management-of-type-2-diabetes-and-its-complications/diabetic-cardiomyopathy.

Pappachan JM, Varughese GI, Sriraman R, Arunagirinathan G. Diabetic cardiomyopathy: pathology, diagnostic evaluation and management. World J diabetes. 2013;4:177-89.

Ciccone MM, Scicchitano P, Cameli M, Cecere A, Cortese F, Dentamaro I, et al. Endothelial dysfunction in pre-diabetes, diabetes and diabetic cardiomyopathy: a review. J Diabetes Metab. 2014;5:1-10.

Diabetic cardiomyopathy-a non coronary complication of diabetes mellitus. Medicine update, 2010. Available at http://www.apiindia.org/pdf/ medicine_update_2010/cardiology_36.pdf. Accessed 30 April 2015

Mitchell RN. Heart. In: Kumar V, Abbas AK, Aster JC, eds. Robbin’s basic pathology.9th edition. Philadelphia: Elsevier, 2013; 365-406.

Haq MAU, Mutha V, Rudd N, Wong C. Diabetic cardiomyopathy- what do we know about it?. World J Cardiovasc Dis. 2013;3:26-32.

Hayat SA, Patel B, Khattar RS, Malik RA. Diabetic cardiomyopathy: mechanisms, diagnosis and treatment. Clin Sci. 2004;107:539-57.

Trachanas K, Sideris S, Aggeli C, Poulidakis E, Gatzoulis K, Tousoulis D. Diabetic cardiomyopathy: from pathophysiology to treatment. Hellenic J Cardiol. 2014;55:411-21.

Voulgari C, Papadogiannis D, Tentolouris N. Diabetic cardiomyopathy: from the pathophysiology of the cardiac myocytes to current diagnosis and management strategies. Vasc Health Risk Manag. 2010;6:883-903.

Boudina S, Abel ED. Diabetic cardiomyopathy revisited. Circulation. 2007;115:3213-23.

Liu Q, Wang S, Cai L. Diabetic cardiomyopathy and its mechanism: role of oxidative stress and damage. J Diabetes Investg 2014;5:623-34.

Poornima IG, Parikh P, Shannon RP. Diabetic cardiomyopathy the search for a unifying hypothesis. Circ Res. 2006;98:596-605.

Mishra TK, Rath PK. Diabetic cardiomyopathy: evidences, pathophysiology and therapeutic considerations. JIACM. 2005;6:312-8.

Wang J, Song Y, Wang Q, Kralik PM, Epstein PN. Causes and characteristics of diabetic cardiomyopathy. Rev Diabetic Stud. 2006;3:108-17.

Chavali V, Tyagi SC, Mishra PK. Predictors and prevention of diabetic cardiomyopathy. Diabetes, Metabolic syndrome and obesity: Targets and therapy. 2013;6:151-60.

Fuentes-Antras J, Ioan AM, Egido J, Lorenzo O. Activation of toll-like receptors and inflammasome complexes in the diabetic cardiomyopathy-associated inflammation. Int J Endocrinol. 2014;2014:1-10.

Chen J, Zhang Z, Cai L. Diabetic cardiomyopathy and its prevention by NrF2: current status. Diabetes Metab J. 2014;38:337-45.

Bugger H, Abel ED. Molecular mechanisms of diabetic cardiomyopathy. Diabetologia. 2014;57:660-71.

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Published

2017-01-10

How to Cite

Barman, C., Pandey, R., Singh, J., & Sodhi, K. S. (2017). Molecular insights into diabetic cardiomyopathy. International Journal of Research in Medical Sciences, 3(7), 1564–1570. https://doi.org/10.18203/2320-6012.ijrms20150230

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Section

Review Articles