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1 , ischemic heart disease, heart failure, and diabetic cardiomyopathy).
2 ucose uptake, with potential implications in diabetic cardiomyopathy.
3 myocardial protection is a major feature of diabetic cardiomyopathy.
4 ntal mechanism underlying the development of diabetic cardiomyopathy.
5 -Glc-NAcylation, plays in the development of diabetic cardiomyopathy.
6 diac myocyte function and the development of diabetic cardiomyopathy.
7 ipid-lowering strategies in the treatment of diabetic cardiomyopathy.
8 on, and reveals a new therapeutic target for diabetic cardiomyopathy.
9 play an important role in the development of diabetic cardiomyopathy.
10 t NO pathway abnormalities may contribute to diabetic cardiomyopathy.
11 disease and is attributed to the presence of diabetic cardiomyopathy.
12 unction is underdiagnosed in early stages of diabetic cardiomyopathy.
13 s an important factor in the pathogenesis of diabetic cardiomyopathy.
14 art and contribute to the pathophysiology of diabetic cardiomyopathy.
15 ogical approaches protects the heart against diabetic cardiomyopathy.
16 de a new plausible biochemical mechanism for diabetic cardiomyopathy.
17 tributes to mitochondrial dysfunction and to diabetic cardiomyopathy.
18 resents a new possible strategy for treating diabetic cardiomyopathy.
19 . 20 +/- 2), which are in keeping with early diabetic cardiomyopathy.
20 ufficient to mitigate streptozotocin-induced diabetic cardiomyopathy.
21 erapy for the treatment and/or prevention of diabetic cardiomyopathy.
22 ions in mitochondrial function contribute to diabetic cardiomyopathy.
23 pathway that can modulate the development of diabetic cardiomyopathy.
24 decline in ventricular function observed in diabetic cardiomyopathy.
25 nt spacing underlie the early development of diabetic cardiomyopathy.
26 autophagy contributes to the pathogenesis of diabetic cardiomyopathy.
27 function and a novel therapeutic strategy in diabetic cardiomyopathy.
28 type 5 inhibitor, sildenafil, in a model of diabetic cardiomyopathy.
29 2 diabetes, obesity, fatty liver disease and diabetic cardiomyopathy.
30 evaluate a possible role of FoxO proteins in diabetic cardiomyopathy.
31 ling pathways, using a mouse model of type 1 diabetic cardiomyopathy.
32 y are important events in the development of diabetic cardiomyopathy.
33 AMPK may represent a novel approach to treat diabetic cardiomyopathy.
34 icular hypertrophy, myocardial ischemia, and diabetic cardiomyopathy.
35 entral role for mitochondrial dysfunction in diabetic cardiomyopathy.
36 ardiac fibrosis is an important component of diabetic cardiomyopathy.
37 n precipitating mitochondrial dysfunction in diabetic cardiomyopathy.
38 f early-phase cardiac cell death can prevent diabetic cardiomyopathy.
39 tent antioxidant prevents the development of diabetic cardiomyopathy.
40 an alternative therapeutic approach to treat diabetic cardiomyopathy.
41 significant prevention of the development of diabetic cardiomyopathy.
42 te to the development of cardiac fibrosis in diabetic cardiomyopathy.
43 plays a critical role in the pathogenesis of diabetic cardiomyopathy.
44 pha (PPAR-alpha) were examined as a model of diabetic cardiomyopathy.
45 hophysiological findings similar to those in diabetic cardiomyopathy.
46 ism and reduced glycolysis may contribute to diabetic cardiomyopathy.
47 Prolongation of relaxation is a hallmark of diabetic cardiomyopathy.
48 been observed, although not consistently, in diabetic cardiomyopathy and are not fully explained by t
51 resent a promising strategy for treatment of diabetic cardiomyopathy and implies therapeutic efficacy
52 ivation of FoxO1 is an important mediator of diabetic cardiomyopathy and is a promising therapeutic t
53 udy examined the effects of SEP and L-Cit on diabetic cardiomyopathy and ischemia/reperfusion injury
54 Co-administration of SEP and L-Cit limits diabetic cardiomyopathy and ischemia/reperfusion injury
55 le for core 2 GlcNAc-T in the development of diabetic cardiomyopathy and modulation of the MAP kinase
56 diabetic drug should extend to treatments of diabetic cardiomyopathy and other cardiovascular disease
57 ling pathways, using a mouse model of type I diabetic cardiomyopathy and primary human cardiomyocytes
58 ts with diabetes exhibit a high incidence of diabetic cardiomyopathy and vascular complications, whic
59 function of the heart, the understanding of 'diabetic cardiomyopathy' and its treatment in humans rem
61 a alters cardiac function and often leads to diabetic cardiomyopathy as cardiomyocyte apoptosis cause
62 s a likely explanation for the transition to diabetic cardiomyopathy as well as to the protection aff
63 Ang 1-7 represents a promising therapy for diabetic cardiomyopathy associated with type 2 diabetes
64 ion of cardiovascular pathologies, including diabetic cardiomyopathy, atherosclerosis, damage from is
65 lay an important role in the pathogenesis of diabetic cardiomyopathy by facilitating MAPK activation,
66 ized that AMPK-induced autophagy ameliorates diabetic cardiomyopathy by inhibiting cardiomyocyte apop
67 sought to characterize the early features of diabetic cardiomyopathy by magnetic resonance imaging (M
68 t activation of PKC signaling contributes to diabetic cardiomyopathy by mechanisms that are poorly un
69 rcise equally ameliorated the development of diabetic cardiomyopathy by preventing LV remodeling and
70 These results suggest that the prevention of diabetic cardiomyopathy by zinc supplementation is predo
76 n of NFE2-related factor 2 (Nrf2) to prevent diabetic cardiomyopathy (DCM), male db/db and age-matche
78 ed TGF-beta activation in the development of diabetic cardiomyopathy exacerbated by abdominal aortic
81 letal muscle and provides protection against diabetic cardiomyopathy; however, it is not known if enh
82 nary bypass grafts, coronary artery disease, diabetic cardiomyopathy, hypertension, ischemia, thrombo
87 myocardial metabolism in the pathogenesis of diabetic cardiomyopathy, insulinopenic mice with PPARalp
89 destiny of CPCs raises the possibility that diabetic cardiomyopathy is a stem cell disease in which
101 diabetic patients is cardiovascular disease; diabetic cardiomyopathy is typified by alterations in ca
104 h clinical studies suggest the existence of 'diabetic cardiomyopathy', it is still difficult to prove
105 ing transgenic (MT-TG) mice are resistant to diabetic cardiomyopathy largely because of the antiapopt
106 the metabolic and functional derangements of diabetic cardiomyopathy, mice with cardiac-restricted ov
109 ging consistent with nonischemic, nonfailing diabetic cardiomyopathy (reduced circumferential strain
112 eexisting congestive heart failure caused by diabetic cardiomyopathy, severe coronary artery disease,
113 fied a novel beneficial effect of Ang 1-7 on diabetic cardiomyopathy that involved a reduction in car
114 ufficient to mitigate streptozotocin-induced diabetic cardiomyopathy through attenuation of oxidative
115 her zinc supplementation can protect against diabetic cardiomyopathy through cardiac MT induction.
116 may be an important mechanism for preventing diabetic cardiomyopathy via AMPK activation that restore
117 is, we tested whether streptozotocin-induced diabetic cardiomyopathy was attenuated in IGF-1 transgen
121 ncreased antioxidant protection could reduce diabetic cardiomyopathy, we assessed cardiac morphology
122 nto the mechanism driving the development of diabetic cardiomyopathy, we studied a unique model of T2
123 ic state, the predominant lipid hallmarks of diabetic cardiomyopathy were each present concomitantly,
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