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Jaetaek Kim  (Kim J) 4 Articles
Basic Research
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Application of Animal Models in Diabetic Cardiomyopathy
Wang-Soo Lee, Jaetaek Kim
Diabetes Metab J. 2021;45(2):129-145.   Published online March 25, 2021
DOI: https://doi.org/10.4093/dmj.2020.0285
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  • 13 Web of Science
  • 16 Crossref
Graphical AbstractGraphical Abstract AbstractAbstract PDFPubReader   ePub   
Diabetic heart disease is a growing and important public health risk. Apart from the risk of coronary artery disease or hypertension, diabetes mellitus (DM) is a well-known risk factor for heart failure in the form of diabetic cardiomyopathy (DiaCM). Currently, DiaCM is defined as myocardial dysfunction in patients with DM in the absence of coronary artery disease and hypertension. The underlying pathomechanism of DiaCM is partially understood, but accumulating evidence suggests that metabolic derangements, oxidative stress, increased myocardial fibrosis and hypertrophy, inflammation, enhanced apoptosis, impaired intracellular calcium handling, activation of the renin-angiotensin-aldosterone system, mitochondrial dysfunction, and dysregulation of microRNAs, among other factors, are involved. Numerous animal models have been used to investigate the pathomechanisms of DiaCM. Despite some limitations, animal models for DiaCM have greatly advanced our understanding of pathomechanisms and have helped in the development of successful disease management strategies. In this review, we summarize the current pathomechanisms of DiaCM and provide animal models for DiaCM according to its pathomechanisms, which may contribute to broadening our understanding of the underlying mechanisms and facilitating the identification of possible new therapeutic targets.

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The Effects of Green Tea on Obesity and Type 2 Diabetes
Hyun Min Kim, Jaetaek Kim
Diabetes Metab J. 2013;37(3):173-175.   Published online June 14, 2013
DOI: https://doi.org/10.4093/dmj.2013.37.3.173
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  • 20 Crossref
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Citations

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Nutritional Status and Cardiac Autophagy
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Diabetes Metab J. 2013;37(1):30-35.   Published online February 15, 2013
DOI: https://doi.org/10.4093/dmj.2013.37.1.30
  • 4,023 View
  • 34 Download
  • 16 Crossref
AbstractAbstract PDFPubReader   

Autophagy is necessary for the degradation of long-lasting proteins and nonfunctional organelles, and is activated to promote cellular survival. However, overactivation of autophagy may deplete essential molecules and organelles responsible for cellular survival. Lifelong calorie restriction by 40% has been shown to increase the cardiac expression of autophagic markers, which suggests that it may have a cardioprotective effect by decreasing oxidative damage brought on by aging and cardiovascular diseases. Although cardiac autophagy is critical to regulating protein quality and maintaining cellular function and survival, increased or excessive autophagy may have deleterious effects on the heart under some circumstances, including pressure overload-induced heart failure. The importance of autophagy has been shown in nutrient supply and preservation of energy in times of limitation, such as ischemia. Some studies have suggested that a transition from obesity to metabolic syndrome may involve progressive changes in myocardial inflammation, mitochondrial dysfunction, fibrosis, apoptosis, and myocardial autophagy.

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Letter: Higher Glycated Hemoglobin Level Is Associated with Increased Risk of Ischemic Stroke in Non-Diabetic Korean Male Adults (Diabetes Metab J 2011;35:551-7)
Seok Hong Lee, Jihyun Ahn, Jaetaek Kim
Diabetes Metab J. 2012;36(1):79-80.   Published online February 17, 2012
DOI: https://doi.org/10.4093/dmj.2012.36.1.79
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