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1 , ischemic heart disease, heart failure, and diabetic cardiomyopathy).
2 ocytes, thereby worsening the progression of diabetic cardiomyopathy.
3 ling pathways, using a mouse model of type 1 diabetic cardiomyopathy.
4 y are important events in the development of diabetic cardiomyopathy.
5 AMPK may represent a novel approach to treat diabetic cardiomyopathy.
6 icular hypertrophy, myocardial ischemia, and diabetic cardiomyopathy.
7 entral role for mitochondrial dysfunction in diabetic cardiomyopathy.
8 ardiac fibrosis is an important component of diabetic cardiomyopathy.
9 n precipitating mitochondrial dysfunction in diabetic cardiomyopathy.
10 f early-phase cardiac cell death can prevent diabetic cardiomyopathy.
11 tent antioxidant prevents the development of diabetic cardiomyopathy.
12 tor 2 (Nrf2) may either ameliorate or worsen diabetic cardiomyopathy.
13 an alternative therapeutic approach to treat diabetic cardiomyopathy.
14 significant prevention of the development of diabetic cardiomyopathy.
15 te to the development of cardiac fibrosis in diabetic cardiomyopathy.
16 plays a critical role in the pathogenesis of diabetic cardiomyopathy.
17 pha (PPAR-alpha) were examined as a model of diabetic cardiomyopathy.
18 hophysiological findings similar to those in diabetic cardiomyopathy.
19 ism and reduced glycolysis may contribute to diabetic cardiomyopathy.
20 Prolongation of relaxation is a hallmark of diabetic cardiomyopathy.
21 myocardial protection is a major feature of diabetic cardiomyopathy.
22 ntal mechanism underlying the development of diabetic cardiomyopathy.
23 -Glc-NAcylation, plays in the development of diabetic cardiomyopathy.
24 diac myocyte function and the development of diabetic cardiomyopathy.
25 ipid-lowering strategies in the treatment of diabetic cardiomyopathy.
26 rategies for the treatment and prevention of diabetic cardiomyopathy.
27 play an important role in the development of diabetic cardiomyopathy.
28 t NO pathway abnormalities may contribute to diabetic cardiomyopathy.
29 disease and is attributed to the presence of diabetic cardiomyopathy.
30 pertension/increased afterload contribute to diabetic cardiomyopathy.
31 epsis-induced cardiomyopathy, arrhythmia and diabetic cardiomyopathy.
32 tionally relevant hiPSC-CM models that mimic diabetic cardiomyopathy.
33 lated pathways and functional derangement of diabetic cardiomyopathy.
34 tial of GCH1/BH4-based therapeutics in human diabetic cardiomyopathy.
35 ic therapeutic modulation of JunD to prevent diabetic cardiomyopathy.
36 linical significance and could contribute to diabetic cardiomyopathy.
37 xis, which contributes to the development of diabetic cardiomyopathy.
38 ifies the myocardial metabolic remodeling in diabetic cardiomyopathy.
39 2 diabetic db/db mice with and without early diabetic cardiomyopathy.
40 tivity and protect the heart from developing diabetic cardiomyopathy.
41 as the core lncRNA with high significance in diabetic cardiomyopathy.
42 l fragment of HDAC4 prevents HDAC4-dependent diabetic cardiomyopathy.
43 t the heart from developing obesity-mediated diabetic cardiomyopathy.
44 tivity and protect the heart from developing diabetic cardiomyopathy.
45 and lipid accumulation, thereby exacerbating diabetic cardiomyopathy.
46 on of mitophagy protects against HFD-induced diabetic cardiomyopathy.
47 art and contribute to the pathophysiology of diabetic cardiomyopathy.
48 ions in mitochondrial function contribute to diabetic cardiomyopathy.
49 2 diabetes, obesity, fatty liver disease and diabetic cardiomyopathy.
50 ucose uptake, with potential implications in diabetic cardiomyopathy.
51 on, and reveals a new therapeutic target for diabetic cardiomyopathy.
52 unction is underdiagnosed in early stages of diabetic cardiomyopathy.
53 s an important factor in the pathogenesis of diabetic cardiomyopathy.
54 ogical approaches protects the heart against diabetic cardiomyopathy.
55 de a new plausible biochemical mechanism for diabetic cardiomyopathy.
56 lying mechanisms and early interventions for diabetic cardiomyopathy.
57 tributes to mitochondrial dysfunction and to diabetic cardiomyopathy.
58 resents a new possible strategy for treating diabetic cardiomyopathy.
59 . 20 +/- 2), which are in keeping with early diabetic cardiomyopathy.
60 ufficient to mitigate streptozotocin-induced diabetic cardiomyopathy.
61 erapy for the treatment and/or prevention of diabetic cardiomyopathy.
62 pathway that can modulate the development of diabetic cardiomyopathy.
63 decline in ventricular function observed in diabetic cardiomyopathy.
64 nt spacing underlie the early development of diabetic cardiomyopathy.
65 autophagy contributes to the pathogenesis of diabetic cardiomyopathy.
66 function and a novel therapeutic strategy in diabetic cardiomyopathy.
67 type 5 inhibitor, sildenafil, in a model of diabetic cardiomyopathy.
68 evaluate a possible role of FoxO proteins in diabetic cardiomyopathy.
69 ral and functional changes that characterize diabetic cardiomyopathy, a complex underlying, and inter
70 been observed, although not consistently, in diabetic cardiomyopathy and are not fully explained by t
72 the mechanisms underlying the development of diabetic cardiomyopathy and heart failure in type 1 and
73 ncRNAs in type 2 mice with and without early diabetic cardiomyopathy and identifies BC038927, G730013
75 resent a promising strategy for treatment of diabetic cardiomyopathy and implies therapeutic efficacy
76 ny cellular mechanisms in multiple models of diabetic cardiomyopathy and in human hearts have been de
77 ivation of FoxO1 is an important mediator of diabetic cardiomyopathy and is a promising therapeutic t
78 udy examined the effects of SEP and L-Cit on diabetic cardiomyopathy and ischemia/reperfusion injury
79 Co-administration of SEP and L-Cit limits diabetic cardiomyopathy and ischemia/reperfusion injury
80 le for core 2 GlcNAc-T in the development of diabetic cardiomyopathy and modulation of the MAP kinase
81 ith a cardiac or renal stressor, would mimic diabetic cardiomyopathy and nephropathy, respectively.
82 diabetic drug should extend to treatments of diabetic cardiomyopathy and other cardiovascular disease
83 lar pathways involved in the pathogenesis of diabetic cardiomyopathy and potential cardioprotective s
84 ling pathways, using a mouse model of type I diabetic cardiomyopathy and primary human cardiomyocytes
85 ices of functional capacity in patients with diabetic cardiomyopathy and stage B heart failure (HF) h
86 is a critical mediator of the progression of diabetic cardiomyopathy and suggest the therapeutic pote
87 ts with diabetes exhibit a high incidence of diabetic cardiomyopathy and vascular complications, whic
88 function of the heart, the understanding of 'diabetic cardiomyopathy' and its treatment in humans rem
90 ing the progression of the disease; in fact, diabetic cardiomyopathies are the main cause of death in
93 a alters cardiac function and often leads to diabetic cardiomyopathy as cardiomyocyte apoptosis cause
94 s a likely explanation for the transition to diabetic cardiomyopathy as well as to the protection aff
95 Ang 1-7 represents a promising therapy for diabetic cardiomyopathy associated with type 2 diabetes
97 ion of cardiovascular pathologies, including diabetic cardiomyopathy, atherosclerosis, damage from is
98 lay an important role in the pathogenesis of diabetic cardiomyopathy by facilitating MAPK activation,
99 hy and suggest the therapeutic potential for diabetic cardiomyopathy by harnessing NAD(+) metabolism.
100 ized that AMPK-induced autophagy ameliorates diabetic cardiomyopathy by inhibiting cardiomyocyte apop
101 sought to characterize the early features of diabetic cardiomyopathy by magnetic resonance imaging (M
102 t activation of PKC signaling contributes to diabetic cardiomyopathy by mechanisms that are poorly un
103 rcise equally ameliorated the development of diabetic cardiomyopathy by preventing LV remodeling and
104 These results suggest that the prevention of diabetic cardiomyopathy by zinc supplementation is predo
105 iabetes leads to a more rapid development of diabetic cardiomyopathy (dbCM) and progression to heart
106 ize exercise capacity among individuals with diabetic cardiomyopathy (DbCM) and reduced peak oxygen u
112 cific form of cardiomyopathy, referred to as diabetic cardiomyopathy (DbCM), originally defined as ve
115 ts with diabetes are at an increased risk of diabetic cardiomyopathy (DCM) and acute myocardial infar
116 traps (NETs), and inflammasome activation in diabetic cardiomyopathy (DCM) and kidney disease (DKD).
117 tigated the effects of astaxanthin (ASTA) on diabetic cardiomyopathy (DCM) and nephropathy (DN) in ra
123 n of NFE2-related factor 2 (Nrf2) to prevent diabetic cardiomyopathy (DCM), male db/db and age-matche
126 -cTnI >=31 ng/L), and echocardiography-based diabetic cardiomyopathy (echo-DbCM; left atrial enlargem
127 ed TGF-beta activation in the development of diabetic cardiomyopathy exacerbated by abdominal aortic
130 t research attention this phenomenon, termed diabetic cardiomyopathy, has received over several decad
131 The pathogenesis and clinical features of diabetic cardiomyopathy have been well-studied in the pa
133 letal muscle and provides protection against diabetic cardiomyopathy; however, it is not known if enh
134 nary bypass grafts, coronary artery disease, diabetic cardiomyopathy, hypertension, ischemia, thrombo
138 MHC-PPAR hearts exhibited signatures of diabetic cardiomyopathy including ventricular hypertroph
139 ions have been described as being altered in diabetic cardiomyopathies, including impaired energy met
141 myocardial metabolism in the pathogenesis of diabetic cardiomyopathy, insulinopenic mice with PPARalp
144 destiny of CPCs raises the possibility that diabetic cardiomyopathy is a stem cell disease in which
147 ent of heart mitochondrial subpopulations in diabetic cardiomyopathy is associated with obesity; howe
161 diabetic patients is cardiovascular disease; diabetic cardiomyopathy is typified by alterations in ca
164 h clinical studies suggest the existence of 'diabetic cardiomyopathy', it is still difficult to prove
165 ing transgenic (MT-TG) mice are resistant to diabetic cardiomyopathy largely because of the antiapopt
166 the metabolic and functional derangements of diabetic cardiomyopathy, mice with cardiac-restricted ov
167 suggest that reduced glucose utilization in diabetic cardiomyopathy might defend against glucotoxici
171 ging consistent with nonischemic, nonfailing diabetic cardiomyopathy (reduced circumferential strain
174 eexisting congestive heart failure caused by diabetic cardiomyopathy, severe coronary artery disease,
176 fied a novel beneficial effect of Ang 1-7 on diabetic cardiomyopathy that involved a reduction in car
178 ately produced clinical endpoints related to diabetic cardiomyopathy, the combination of the two did
179 ufficient to mitigate streptozotocin-induced diabetic cardiomyopathy through attenuation of oxidative
180 her zinc supplementation can protect against diabetic cardiomyopathy through cardiac MT induction.
181 can exert an important regulatory effect on diabetic cardiomyopathy through extracellular vesicular
182 may be an important mechanism for preventing diabetic cardiomyopathy via AMPK activation that restore
183 is, we tested whether streptozotocin-induced diabetic cardiomyopathy was attenuated in IGF-1 transgen
189 ncreased antioxidant protection could reduce diabetic cardiomyopathy, we assessed cardiac morphology
190 se delivery and mitochondrial dysfunction in diabetic cardiomyopathy, we generated transgenic mice wi
191 nto the mechanism driving the development of diabetic cardiomyopathy, we studied a unique model of T2
192 ic state, the predominant lipid hallmarks of diabetic cardiomyopathy were each present concomitantly,
193 oratory characteristics of participants with diabetic cardiomyopathy were evaluated using baseline da
195 ich diabetes contributes to the pathology of diabetic cardiomyopathy, which presents as cardiac hyper
196 re, we summarize the molecular mechanisms of diabetic cardiomyopathy, with a special emphasis on card