| REVIEW ARTICLE |
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| Year : 2016 | Volume
: 1
| Issue : 3 | Page : 20-27 |
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Role of the cathepsin K/Calcineurin/Nuclear factor of activated T-cells axis in the pathogenesis and management of diabetic cardiomyopathy
Rui Guo1, Sreejayan Nair1, Jun Ren2
1 Center for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, WY, USA
2 Center for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, WY, USA; Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China
Correspondence Address:
Prof. Jun Ren
Center for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, WY 82071
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/2470-7511.248354
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Diabetes mellitus has become a devastating global epidemic. Patients with diabetes suffer a high prevalence of diabetic cardiomyopathy (DCM). DCM is a type of cardiac problem independent of any preexisting macro- and micro-vascular diseases. The pathophysiological basis underlying diabetes-induced cardiac damage is rather complex and multifactorial. Although a number of risk factors including oxidative stress, apoptosis, and aberrant intracellular Ca2+ metabolism have been postulated to play a role in the onset and development of cardiac anomalies within diabetes, the precise mechanisms responsible for DCM remain elusive. This mini-review discusses the latest findings of mechanisms involved in the progression of cardiomyopathy in diabetes. We emphasize the role of the lysosomal cysteine protease, cathepsin K, and its downstream calcineurin/nuclear factor of activated T-cells signaling in the prevention and treatment of DCM.
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