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1 toward effects, collectively referred to as 'diabetic complications'.
2 ibutes to the intractability of this serious diabetic complication.
3 Diabetic neuropathy is the most common diabetic complication.
4 as being responsible for development of this diabetic complication.
5 t endothelial function from dyslipidemia and diabetic complications.
6 open new avenues for targeting human FN3K in diabetic complications.
7 might also participate in the development of diabetic complications.
8 n enzyme to deglycate proteins implicated in diabetic complications.
9 ixture and high rates of type 2 diabetes and diabetic complications.
10 sociated with type 1 and type 2 diabetes and diabetic complications.
11 volvement in development of various vascular diabetic complications.
12 dent risk factor for development of vascular diabetic complications.
13 rsued for treatment of microvascular-related diabetic complications.
14 s being critical for prevention of long-term diabetic complications.
15 factor influencing the development of major diabetic complications.
16 ing disorders are at high risk of developing diabetic complications.
17 ia their receptor, RAGE, play major roles in diabetic complications.
18 way, is a promising approach in treatment of diabetic complications.
19 ) has been implicated in the pathogenesis of diabetic complications.
20 been linked to the development of secondary diabetic complications.
21 ion reportedly found in the target organs of diabetic complications.
22 is an important transcriptional regulator of diabetic complications.
23 etes and (2) to assess their contribution to diabetic complications.
24 uscle cell signal transduction contribute to diabetic complications.
25 been linked to the development of secondary diabetic complications.
26 thought to contribute to the pathogenesis of diabetic complications.
27 ntial therapeutic roles in the prevention of diabetic complications.
28 reases the incidence of diabetes and worsens diabetic complications.
29 t Smad signaling may play a critical role in diabetic complications.
30 through the receptor for AGEs, contribute to diabetic complications.
31 heir receptor, RAGE, to play a major role in diabetic complications.
32 little effect on the development of T2D and diabetic complications.
33 optimal for finding susceptibility genes for diabetic complications.
34 mation and protection against development of diabetic complications.
35 e an important factor in the pathogenesis of diabetic complications.
36 rglycemia contributes to the pathogenesis of diabetic complications.
37 been implicated in the etiology of secondary diabetic complications.
38 reactions that are thought to play a role in diabetic complications.
39 y has been implicated in the pathogenesis of diabetic complications.
40 genes that contribute to the pathogenesis of diabetic complications.
41 sm that underlies the development of various diabetic complications.
42 hibitors of AGE formation and development of diabetic complications.
43 tabolic reprogramming in the pathogenesis of diabetic complications.
44 ellular membranes and to the pathogenesis of diabetic complications.
45 parameter most consistently associated with diabetic complications.
46 s, without increased risk of readmission for diabetic complications.
47 mine whether PKC-beta inhibition can prevent diabetic complications.
48 collagen are correlated with the severity of diabetic complications.
49 m glycemic control and a strong predictor of diabetic complications.
50 might contribute to CaMKII-dependent retinal diabetic complications.
51 n initiative, which emphasizes prevention of diabetic complications.
52 has been linked to the pathogenesis of some diabetic complications.
53 detection and correction of risk factors for diabetic complications.
54 ht to contribute to the pathogenesis of many diabetic complications.
55 occur in several diseases states, including diabetic complications.
56 ses, e.g., AIDS, cancer, atherosclerosis and diabetic complications.
57 in vascular cells and tissues susceptible to diabetic complications.
58 ic patients before the development of severe diabetic complications.
59 ss and is associated with the development of diabetic complications.
60 dori-modified proteins in the development of diabetic complications.
61 tablished concomitant factor associated with diabetic complications.
62 c peripheral neuropathy (DPN) are two common diabetic complications.
63 ns of objectively measured and self-reported diabetic complications.
64 the outcomes of HSPC transplantation and of diabetic complications.
65 ong correlation between the test results and diabetic complications.
66 itor cells (HSPCs), which, in turn, predicts diabetic complications.
67 idues of proteins and thereby contributes to diabetic complications.
68 cal trials for the treatment of diabetes and diabetic complications.
69 es and is a potential therapeutic target for diabetic complications.
70 inhibition of ALR2 and possible treatment of diabetic complications.
71 good glycaemic control is essential to delay diabetic complications.
72 nificant biomarker towards the prediction of diabetic complications.
73 ion reactions, which are the major causes of diabetic complications.
74 adical activity underlie the pathogenesis of diabetic complications.
75 of hyperglycemic excursions associated with diabetic complications.
76 s novel benchmarks for the future studies of diabetic complications.
77 a novel therapeutic option for treatment of diabetic complications.
78 , have been implicated in the development of diabetic complications.
79 aradigm shift in our understanding of ocular diabetic complications.
80 production is central to the development of diabetic complications.
81 -documented beneficial preventive effects on diabetic complications.
82 ion of these various factors and less severe diabetic complications.
83 tic patients and is thought to contribute to diabetic complications.
84 new mechanisms underlying the development of diabetic complications.
85 ay contribute to Wnt signaling activation in diabetic complications.
86 for controlling protein glycation associated diabetic complications.
87 st and earlier phase to minimize the risk of diabetic complications.
88 ducts and therefore potentially mitigate the diabetic complications.
89 icyte-endothelial crosstalk in microvascular diabetic complications.
90 ways of using stem cell therapy to overcome diabetic complications.
91 standing the complex pathophysiology of many diabetic complications.
92 fying people at risk of incident diabetes or diabetic complications.
93 usal link between diabetes mellitus (DM) and diabetic complications.
94 way, plays a key role in the pathogenesis of diabetic complications.
95 al cell (EC) dysfunction plays a key role in diabetic complications.
96 besity and metabolic syndrome, diabetes, and diabetic complications.
97 n dysfunction and plays an important role in diabetic complications.
98 d to determine the role of TNFalpha in these diabetic complications.
99 n hyperglycemia is a major mechanism causing diabetic complications.
100 (CARHSP1) was identified as a biomarker for diabetic complications.
101 lele is associated with an increased risk of diabetic complications.
102 tabolite-generated ROS in the development of diabetic complications.
103 Thus, lack of B1R and B2R exacerbates diabetic complications.
104 ly with reference to the effect on long-term diabetic complications.
105 mmation and metabolic memory associated with diabetic complications.
106 d glycation end products play major roles in diabetic complications.
107 g glycation from hyperglycemia as a cause of diabetic complications, a Pseudomonas sp. soil strain co
108 E-mediated diseases, such as those linked to diabetic complications, Alzheimer's disease, and chronic
109 th increased six-month readmission rates for diabetic complications among diabetics and nondiabetics.
111 s as a causative treatment strategy for late diabetic complications and call for a more detailed anal
113 nced glycation end products (AGEs) linked to diabetic complications and cardiovascular diseases.
114 reemptive identification and anticipation of diabetic complications and comorbidities, along with an
115 Monocytes are rapidly recruited to sites of diabetic complications and differentiate into macrophage
116 hways of crucial importance in propensity to diabetic complications and heart disease in the general
117 crucial role in the pathogenesis of multiple diabetic complications and is reportedly induced in the
119 various age-associated pathologies, such as diabetic complications and neurodegenerative disorders l
120 T2D and review the effect of inflammation on diabetic complications and on the relationship between T
121 ns provide new insights into the etiology of diabetic complications and suggest potential novel thera
122 value of HbA1c is its use as a predictor of diabetic complications and the proven effect of improved
123 Impaired macrophage functions imposed by diabetic complications and the suppressed formation of 1
125 -term survival, improvement in the course of diabetic complications, and amelioration of quality of l
126 Levels of HbA1c track epidemiologically with diabetic complications, and glycemic control, as reflect
127 disorders, including Alzheimer disease (AD), diabetic complications, and inflammatory conditions.
128 erosis and vascular remodeling after injury, diabetic complications, and neurodegenerative disorders.
129 omics is a reliable source for biomarkers of diabetic complications, and our data suggest that renal
130 at therapeutic potential in the treatment of diabetic complications, and perhaps other cardiovascular
137 on and cardiac microvascular dysfunction are diabetic complications associated with increased mortali
138 cated in the development of several vascular diabetic complications (atherosclerosis, nephropathy, an
139 mic control, not only to reverse established diabetic complications but also to improve beta-cell sta
140 l decreases the incidence and progression of diabetic complications but increases the incidence of hy
141 elays the onset and slows the progression of diabetic complications but is associated with frequent d
142 ameliorates the progression of microvascular diabetic complications but the procedure is associated w
143 lay a role in many processes underlying late diabetic complications, but efforts to identify genetic
144 fibrosis within 3 months and die because of diabetic complications by 6-7 months after a single inje
145 ent, metformin treatment may protect against diabetic complications by mechanisms independent of its
146 y OGT has been linked to insulin resistance, diabetic complications, cancer and neurodegenerative dis
147 Atherosclerosis, hypertension, obesity, diabetic complications, cancer, benign prostate hyperpla
148 GF therapy may be useful in the treatment of diabetic complications characterized by impaired neovasc
150 he auspices of the NIH, the Animal Models of Diabetic Complications Consortium has worked to address
151 ased O-GlcNAc levels to glucose toxicity and diabetic complications; conversely, acute activation of
152 -dicarbonyl that is thought to contribute to diabetic complications either as a direct toxin or as a
153 , the most common and problematic of chronic diabetic complications, essential for a wide range of me
154 tion end products (AGEs), known promoters of diabetic complications, form abundantly in heated foods
156 t efforts to identify treatments for chronic diabetic complications have resulted in the discovery of
157 chondrial dysfunction has been implicated in diabetic complications; however, it is unknown whether h
158 educing sugars, have been implicated in many diabetic complications; however, their role in diabetic
159 enrichment of AGE-RAGE signaling pathway in diabetic complications, IL-17 signaling, and cysteine an
161 le effectively preventing the development of diabetic complications in animals, results from clinical
162 h aDM, and establishing their importance for diabetic complications in different health system contex
163 nomeric peptide that reduces body weight and diabetic complications in rodent models of obesity by ac
164 GE-DIAPH1 interaction with RAGE229 mitigated diabetic complications in rodents by attenuating inflamm
166 l therapeutic interventions that may prevent diabetic complications in the presence of hyperglycemia,
167 glutathionylation may play a central role in diabetic complications in vivo where Grx1 is increased.
169 uld provide a novel therapeutic approach for diabetic complications including nephropathy, and other
171 which activates major pathways implicated in diabetic complications, including advanced glycation end
172 n has a critical role in the pathogenesis of diabetic complications, including diabetic nephropathy (
173 lucose is a key factor in the development of diabetic complications, including diabetic nephropathy.
174 OD genetic background may predispose them to diabetic complications, including insulin resistance in
175 istent with a multifactorial pathogenesis of diabetic complications, including roles for metabolic im
176 al drug target because of its involvement in diabetic complications, inflammation, and tumorigenesis.
177 , amyloid beta, and HMGB1 has been linked to diabetic complications, inflammatory and neurodegenerati
178 m of diabetes but not the sole cause of late diabetic complications; instead, other diabetes-related
182 ved mechanistic understanding of each of the diabetic complications is needed in order to develop dis
183 e role of aldose reductase (ALR2) in causing diabetic complications is well-studied, with overactivit
184 products is implicated in the development of diabetic complications, little is known about the chemic
186 pathogenesis of various diseases, including diabetic complications, neurodegenerative disorders, and
187 pathogenesis of various diseases, including diabetic complications, neurodegenerative disorders, and
188 development of novel therapeutic options for diabetic complications, neuropathology, and cancer.
189 sorbitol is associated with MI depletion in diabetic complications, no causal relationship has been
190 inhibitors of this enzyme in order to combat diabetic complications, non-selective inhibition of both
192 ng (odds ratio, 1.35; 95% CI, 1.23-1.47) and diabetic complications (odds ratio, 1.35; 95% CI, 1.2-1.
194 etes has become a pandemic and leads to late diabetic complications of organs, including kidney and e
195 United States, but the burden and effect of diabetic complications on this group of people is not fu
196 mechanisms may operate in different types of diabetic complications or at different stages of specifi
197 -2001 who developed NODM was used to examine diabetic complications over the first three years posttr
199 BDM, targeting neutrophilic inflammation and diabetic complication pathways to address the greater mo
200 r 5 (insulin-resistant, 5%) with no dominant diabetic complication patterns; cluster 2 (age-related,
201 amin E, failed to show beneficial effects on diabetic complications probably because their action is
206 sp. of potential relevance for treatment of diabetic complications resulting from excessive protein
208 G6PC2 expression can affect the incidence of diabetic complications, risk for type 2 diabetes mellitu
209 erse array of clinical conditions, including diabetic complications, sepsis, preeclampsia, and athero
210 unction and metabolic inflammation, but also diabetic complications such as diabetic kidney diseases
214 cular risk factors confer increased risk for diabetic complications such as peripheral neuropathy, ne
215 ial barrier function is a salient feature of diabetic complications such as sight-threatening diabeti
216 primary diabetes and its effects on various diabetic complications, such as diabetic cardiovascular
218 iabetes may predispose to the development of diabetic complications, such as infection and impaired h
219 ficantly decrease or halt the progression of diabetic complications, support the continued applicatio
221 Maternal diabetes-induced NTDs are severe diabetic complications that lead to infant mortality or
222 in the study of atherosclerosis and of other diabetic complications, the consortium has created a sys
223 vestigated to understand the pathogenesis of diabetic complications, the increased metabolism of gluc
224 ase, an enzyme linked to the pathogenesis of diabetic complications, the physiological role of FR-1 i
225 patients who would be most likely to develop diabetic complications, thereby both improving patient h
226 been widely studied for their involvement in diabetic complications; these complications are largely
227 enic role of PKCbetaII in the development of diabetic complications, this structure can serve as a te
228 ditis, heart failure, circulatory shock, and diabetic complications to atherosclerosis, arthritis, co
229 increased rates of hospital readmission for diabetic complications traditionally associated with bet
231 nd degree of risk factor control with common diabetic complications using data from the UK Biobank (n
232 act by activating Smad signaling to mediate diabetic complications via both TGF-beta-dependent and -
233 After adjustment for other risk factors and diabetic complications, we found that duration of diabet
234 ole of phagocytic superoxide in the onset of diabetic complications, we used a model of periodontitis
235 ol (hemoglobin A1c [HbA1c]), and presence of diabetic complications were determined at recruitment.
237 climb, the number of individuals living with diabetic complications will reach an unprecedented magni
239 nd products (AGEs) have an important role in diabetic complications, with many responses mediated thr
240 the oral glucose tolerance test all predict diabetic complications yet test reliability is better fo