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1 f congestive heart failure, hypertension, or diabetic nephropathy.
2 nvolved in the pathogenesis and treatment of diabetic nephropathy.
3 o first-in-human trials for the treatment of diabetic nephropathy.
4 an clinical trials in patients with NASH and diabetic nephropathy.
5 activators were pursued for the treatment of diabetic nephropathy.
6 complications and the role of these AGEs in diabetic nephropathy.
7 e renoprotective effects of Glp1r agonism in diabetic nephropathy.
8 , play a critical role in the development of diabetic nephropathy.
9 stress is emerging as a critical mediator of diabetic nephropathy.
10 or the therapeutic effects of fenofibrate on diabetic nephropathy.
11 urine were reduced in patients with advanced diabetic nephropathy.
12 HIF-1 may improve clinical manifestations of diabetic nephropathy.
13 ression of IL-17A was sufficient to suppress diabetic nephropathy.
14 ssing and thereby upregulating NOX4 in early diabetic nephropathy.
15 volved in processing of miRNAs implicated in diabetic nephropathy.
16 uctase inhibitors have been shown to improve diabetic nephropathy.
17 e strongly associated with susceptibility to diabetic nephropathy.
18 einuria and renal damage during experimental diabetic nephropathy.
19 ns of reduced albuminuria with atrasentan in diabetic nephropathy.
20 owering drug, Ezetimibe (EZT) on severity of diabetic nephropathy.
21 Here, we examined the role of IL-17A in diabetic nephropathy.
22 effects of the VEGF-A isoform VEGF-A165b in diabetic nephropathy.
23 ays that mediate podocyte injury and loss in diabetic nephropathy.
24 d functional and histologic abnormalities in diabetic nephropathy.
25 lium to protect blood vessels and ameliorate diabetic nephropathy.
26 d severe podocyte effacement, matching human diabetic nephropathy.
27 s are significantly elevated in experimental diabetic nephropathy.
28 versely with renal function in patients with diabetic nephropathy.
29 el therapeutic strategy for the treatment of diabetic nephropathy.
30 s whereby 20-HETE affects the progression of diabetic nephropathy.
31 orylation, which may, in turn, contribute to diabetic nephropathy.
32 on of angiogenic VEGF-A isoforms each worsen diabetic nephropathy.
33 ress, suggesting a possible role for ASK1 in diabetic nephropathy.
34 nd nitration is linked to the development of diabetic nephropathy.
35 s cardinal signatures for the development of diabetic nephropathy.
36 thelial Adora2b signaling in protection from diabetic nephropathy.
37 lin effects in podocytes during experimental diabetic nephropathy.
38 barrier homeostasis and are dysregulated in diabetic nephropathy.
39 ing diffuse glomerulosclerosis, particularly diabetic nephropathy.
40 erged as a novel target for the treatment of diabetic nephropathy.
41 itical mediator of podocyte injury in type 2 diabetic nephropathy.
42 signaling of extracellular adenosine during diabetic nephropathy.
43 owed a selective induction of Adora2b during diabetic nephropathy.
44 e heart failure, ventricular remodeling, and diabetic nephropathy.
45 ory bowel disease, rheumatoid arthritis, and diabetic nephropathy.
46 cleotide polymorphisms at the B7-1 gene with diabetic nephropathy.
47 strategy for the prevention or treatment of diabetic nephropathy.
48 dora2b signaling in kidney protection during diabetic nephropathy.
49 between lupus nephritis, IgA nephritis, and diabetic nephropathy.
50 resent early markers of glomerular injury in diabetic nephropathy.
51 receptors (EGFRs) are activated in models of diabetic nephropathy.
52 c may provide a novel therapeutic target for diabetic nephropathy.
53 ofiles differ across the different stages of diabetic nephropathy.
54 or therapeutic intervention in patients with diabetic nephropathy.
55 vitro and in vivo disease models, including diabetic nephropathy.
56 n was observed in podocytes of patients with diabetic nephropathy.
57 xpression directly modulates the severity of diabetic nephropathy.
58 ar protease aPC to mitochondrial function in diabetic nephropathy.
59 contributes to tubulointerstitial changes in diabetic nephropathy.
60 mesangial hypertrophy in the progression of diabetic nephropathy.
61 s to metabolic disease complications such as diabetic nephropathy.
62 d risk of adverse events among patients with diabetic nephropathy.
63 he beneficial effects of aPC in experimental diabetic nephropathy.
64 at the EP1 receptor promotes renal damage in diabetic nephropathy.
65 tissue from patients with varying degrees of diabetic nephropathy.
66 strategy in the prevention and treatment of diabetic nephropathy.
67 nt of renal fibrosis in two animal models of diabetic nephropathy.
68 to the prediction of progression to clinical diabetic nephropathy.
69 tients with chronic kidney disease (CKD) and diabetic nephropathy.
70 -regulating protein p66(Shc) in experimental diabetic nephropathy.
71 cy of RAAS inhibitors in promoting repair of diabetic nephropathy.
72 and the EP1 receptor could be beneficial in diabetic nephropathy.
73 Glomerular hypertrophy is a hallmark of diabetic nephropathy.
74 eactive oxygen species) measures of advanced diabetic nephropathy.
75 ributes to the tubulointerstitial lesions of diabetic nephropathy.
76 ous TLR4 ligand high-mobility group box 1 in diabetic nephropathy.
77 ng represent early kidney responses in human diabetic nephropathy.
78 hypertension, congestive heart failure, and diabetic nephropathy.
79 esion formation in tissue from patients with diabetic nephropathy.
80 , informing a potential approach to treating diabetic nephropathy.
81 lomerular structure and function and lost in diabetic nephropathy.
82 ture and function in a mouse model of severe diabetic nephropathy.
83 itors as a therapeutic target in people with diabetic nephropathy.
84 es and is considered a risk factor for later diabetic nephropathy.
85 l cell (GEnC) dysfunction and albuminuria in diabetic nephropathy.
86 for future investigation in the treatment of diabetic nephropathy.
87 cumulation, two key pathologic signatures of diabetic nephropathy.
88 itulating the phenotype of progressive human diabetic nephropathy.
89 d in renal biopsies from human subjects with diabetic nephropathy.
90 t among children who are already at risk for diabetic nephropathy.
91 Risk of death was higher among patients with diabetic nephropathy.
92 igation as a novel renoprotective therapy in diabetic nephropathy.
93 n implicated as a major pathogenic factor in diabetic nephropathy.
94 FSGS, IgA nephropathy, lupus nephritis, and diabetic nephropathy.
95 its derived ROS in promoting progression of diabetic nephropathy.
96 of PKM2 protects mitochondrial integrity in diabetic nephropathy.
97 actor-1alpha relevant in the pathogenesis of diabetic nephropathy.
98 ia, which is involved in the pathogenesis of diabetic nephropathy.
99 f a wide range of kidney diseases, including diabetic nephropathy.
100 protein levels in human and animal models of diabetic nephropathy.
101 ystem inhibitors did not slow progression of diabetic nephropathy.
102 sting a therapeutic potential for NOX-E36 in diabetic nephropathy.
103 long-lasting albuminuria-reducing effects in diabetic nephropathy.
104 y significant difference in survival between diabetic nephropathy (23.8%) and other patients with CKD
105 in kidney disease, including podocytopathy, diabetic nephropathy, albuminuria, autosomal dominant po
106 lmost abolishes the pathological features of diabetic nephropathy, although it does not affect the hy
107 milar NMDA antagonist memantine also reduced diabetic nephropathy, although it was less effective tha
108 has been proposed to be a unifying cause for diabetic nephropathy and a target for novel therapies.
109 pathway, a key factor in the development of diabetic nephropathy and an inhibitor of autophagy, is i
110 pertension and podocyte injury contribute to diabetic nephropathy and are strong predictors of diseas
111 kidney and in pathologic conditions such as diabetic nephropathy and CKD; upregulation of Nox4 may b
112 c variation influence the risk of developing diabetic nephropathy and ESRD in patients with type 1 di
113 indicate that excess sema3a promotes severe diabetic nephropathy and identifies novel potential ther
115 show that renal Nox5 is upregulated in human diabetic nephropathy and may alter filtration barrier fu
117 lear bile acid receptor in the prevention of diabetic nephropathy and obesity-induced renal damage.
119 hogenesis of several renal diseases, such as diabetic nephropathy and polycystic kidney disease.
120 ) has been implicated in the pathogenesis of diabetic nephropathy and renal fibrosis; however, the ca
121 podocytes contributes to the development of diabetic nephropathy and represents a common pathway thr
122 lications, including cardiovascular disease, diabetic nephropathy and retinopathy, have a negative ef
124 inuria and glomerulosclerosis (indicators of diabetic nephropathy) and attenuated albumin leakage int
125 proteinuria in two independent mouse models, diabetic nephropathy, and adriamycin-induced nephropathy
126 important role in the development of type 1 diabetic nephropathy, and its inhibition could be a prom
128 Adora2b(-/-) mice experienced more severe diabetic nephropathy, and studies in mice with tissue-sp
129 d PKC-beta contribute to the pathogenesis of diabetic nephropathy, and that dual inhibition of the cl
130 also induced in vivo in two murine models of diabetic nephropathy, and treatment with CTLA4-Ig preven
131 abetic fatty rats and patients with advanced diabetic nephropathy, and were normalized by pharmacolog
133 meruli of patients with early and late-stage diabetic nephropathy, as well as other nondiabetic glome
134 minant polycystic kidney disease (ADPKD) and diabetic nephropathy associated with higher HRs for mort
135 the hypothesis of a reactive rise of ADM in diabetic nephropathy, blunted in risk alleles carriers,
136 diabetic mice developed the full picture of diabetic nephropathy, but diabetic retinopathy was preve
137 y and resulting albuminuria are hallmarks of diabetic nephropathy, but targeted therapies to halt or
138 a is a major pathogenic factor that promotes diabetic nephropathy, but the underlying mechanism remai
139 , we wanted to explore the role of Ang II in diabetic nephropathy by a translational approach spannin
140 ranscription (STAT) signaling contributes to diabetic nephropathy by inducing genes involved in leuko
141 for early atherosclerosis, type 2 diabetes, diabetic nephropathy, cardiovascular disease and all-cau
142 Chronic exposure to high glucose leads to diabetic nephropathy characterized by increased mesangia
144 standard methods, including determination of diabetic nephropathy class, as defined by the Renal Path
145 , and human kidney tissue from patients with diabetic nephropathy demonstrated lower gene expression
148 ranoproliferative glomerulonephritis (MPGN), diabetic nephropathy (DN) and obesity-related glomerulop
149 Loss of podocytes is an early feature of diabetic nephropathy (DN) and predicts its progression.
150 n, and with the global epidemic of diabetes, diabetic nephropathy (DN) became the leading cause of en
153 nt normoalbuminuria and 162 individuals with diabetic nephropathy (DN) from the outpatient clinic at
157 particularly relevant to the pathogenesis of diabetic nephropathy (DN) in which evidence suggests tha
167 re particularly vulnerable to development of Diabetic nephropathy (DN) leading to End Stage Renal Dis
168 sized that proteases aberrantly expressed in diabetic nephropathy (DN) may be involved in the generat
170 served mitochondrial protein associated with diabetic nephropathy (DN) that amplifies profibrotic tra
171 t is important to find better treatments for diabetic nephropathy (DN), a debilitating renal complica
172 renal proximal tubule is a site of injury in diabetic nephropathy (DN), and progressive renal tubuloi
173 mic reticulum (ER) stress is associated with diabetic nephropathy (DN), but its pathophysiological re
174 helial cells (PTECs) has been highlighted in diabetic nephropathy (DN), but little is known about the
175 instruments in defining the pathogenesis of diabetic nephropathy (DN), but they only partially recap
176 We analyzed specimens from patients with diabetic nephropathy (DN), FSGS, IgA nephropathy (IgAN),
177 As high glucose and oxidative stress mediate diabetic nephropathy (DN), the contribution of TxNIP was
179 k factor in the pathogenesis of both CVD and diabetic nephropathy (DN), with CVD identified as the pr
180 lications of diabetes and obesity, including diabetic nephropathy (DN), without any US Food and Drug
181 proach to assess the functional context of a diabetic nephropathy (DN)-associated SNP located in the
199 A-L) prevented lipid-induced renal injury in diabetic nephropathy (DN). However, the role and regulat
200 (n = 6839), type 2 diabetes (T2D; n = 7710), diabetic nephropathy (DN; n = 2452), % body fat (n = 555
201 fit of Nrf2 activation and ROS inhibition in diabetic nephropathy (dNP), the Nrf2 activator bardoxolo
203 s with focal segmental glomerulosclerosis or diabetic nephropathy exhibited diminished H3K27me3 and h
204 psies from patients with IgA nephropathy and diabetic nephropathy exhibited substantial activation of
205 et were significantly less likely to develop diabetic nephropathy, exhibiting less albuminuria, glome
206 mL/min per 1.73m(2), or development of overt diabetic nephropathy), eye events (a composite of requir
207 and the damaged rat mesangial cells leads to diabetic nephropathy, fibrosis, and proteinurea, which a
208 n a cohort of 3652 patients from the Finnish Diabetic Nephropathy (FinnDiane) Study with type 1 diabe
210 nge 0-2.9 microM for patients with diagnosed diabetic nephropathy, gout or hyperuricemia, and can rea
213 docyte membrane component that is reduced in diabetic nephropathy, has been shown to activate phospho
214 Cardiovascular Outcomes in Participants with Diabetic Nephropathy) have shown that the sodium-glucose
215 ubunit of N-type calcium channel, Cav2.2, in diabetic nephropathy, however, remains to be clarified.
217 in common human glomerulopathies, including diabetic nephropathy, IgA nephropathy, and lupus nephrit
218 -1 blockade attenuates the manifestations of diabetic nephropathy in a type 1 diabetic animal model,
219 osine kinase activity, on the progression of diabetic nephropathy in a type 1 diabetic mouse model.
220 e myosin heavy chain IIA are associated with diabetic nephropathy in European Americans and with sick
221 Thus, we examined the role of Nox5 in human diabetic nephropathy in human mesangial cells and in an
224 administration of low-dose IL-17A prevented diabetic nephropathy in models of type 1 and type 2 diab
225 ese susceptibility loci were associated with diabetic nephropathy in patients from the Joslin Study o
226 ere independent predictors of progression to diabetic nephropathy in this normoalbuminuric cohort.
227 with erlotinib attenuates the development of diabetic nephropathy in type 1 diabetes, which is mediat
228 ubsequently been shown to be associated with diabetic nephropathy in unrelated patients with type 2 d
229 Nx resulted in several clinical hallmarks of diabetic nephropathy indicative of early disease develop
240 UII and UII receptors (UTR) are increased in diabetic nephropathy, it remains unclear whether UII reg
242 nd -4 in several glomerulopathies, including diabetic nephropathy, little is known regarding the role
243 isease [CD] and ulcerative colitis [UC]) and diabetic nephropathy (macroalbuminuria and end-stage ren
245 of native kidney disease were primary FSGS, diabetic nephropathy, membranous nephropathy, immunoglob
246 affected by Tgfb1 genotype, many features of diabetic nephropathy (mesangial expansion, elevated plas
247 replacing leptin could reverse the advanced diabetic nephropathy modeled by the leptin-deficient BTB
248 ated in autoimmunity-driven type-1 diabetes, diabetic nephropathy, multiple sclerosis, asthma, athero
250 nal vessel calibers as 16-year predictors of diabetic nephropathy, neuropathy, and proliferative reti
251 slowing renal function loss in patients with diabetic nephropathy on chronic stable renin-angiotensin
252 mesangial cells that play a pivotal role in diabetic nephropathy, one of the leading causes of renal
254 rval [CI] = 1.05-50.06) and among those with diabetic nephropathy (OR = 1.65; 95% CI = 1.10-2.48).
257 ached statistical significance with advanced diabetic nephropathy (P = 0.037 [adjusted P = 0.222]).
258 rotective effects against the progression of diabetic nephropathy, partly by protecting podocytes.
259 In summary, VEGFC reduced the development of diabetic nephropathy, prevented VEGF receptor alteration
261 a suggest that EP1 activation contributes to diabetic nephropathy progression at several locations, i
264 cytokines, inhibiting the pathomorphology of diabetic nephropathy, renal lipid accumulation, and impr
267 c overexpression of Nox5 in a mouse model of diabetic nephropathy showed enhanced glomerular ROS prod
268 isoform of NADPH oxidase in animal models of diabetic nephropathy since Nox5 is absent in the mouse g
269 e MPs were assessed in three mouse models of diabetic nephropathy: streptozotocin (STZ)-treated, OVE2
270 collections previously identified four novel diabetic nephropathy susceptibility loci that have subse
274 h glucose paves the way for complications of diabetic nephropathy through the production of reactive
275 dence that KCa3.1 mediates renal fibrosis in diabetic nephropathy through the TGF-beta1/Smad signalin
276 loss of tubular Tyro3 and Mer expression in diabetic nephropathy tissue and glomerular depositions o
278 rotein-protein interactions at each stage of diabetic nephropathy to provide an overview of the event
279 entifies ASK1 as a new therapeutic target in diabetic nephropathy to reduce renal inflammation and fi
281 in- and ischemia/reperfusion-induced injury, diabetic nephropathy, ureteral obstructive disease, and
282 glomerular injury in experimental and human diabetic nephropathy via persistent activation of Notch1
283 he endothelial glycocalyx is also reduced in diabetic nephropathy, we hypothesized that MCP-1 inhibit
284 sms leading to glomerular podocyte injury in diabetic nephropathy, we performed quantitative proteomi
285 sing kidney biopsy sections from people with diabetic nephropathy, we show that Notch signaling is in
286 iber's effect on development of experimental diabetic nephropathy, we used streptozotocin to induce d
289 mbinant human VEGF-A165b reduced features of diabetic nephropathy when initiated during early or adva
291 tion of CD73 was associated with more severe diabetic nephropathy, whereas treatment with soluble nuc
292 number may hold promise in the treatment of diabetic nephropathy, which could eventually lead to app
293 ings showed AS-IV to be beneficial to type 2 diabetic nephropathy, which might be associated with the
294 Earlier detection of progression risk in diabetic nephropathy will allow earlier intervention to
295 l disease (ESRD) worldwide, most people with diabetic nephropathy will never develop ESRD but will in
296 ker diabetic fatty (ZDF) rats develop type 2 diabetic nephropathy with albuminuria, reduced glomerula
297 duce diabetes, wild-type mice developed mild diabetic nephropathy with microalbuminuria, mesangial ma
298 ) has been implicated in the pathogenesis of diabetic nephropathy with proteinuria and peritubular ex
299 cyte dysfunction is a detrimental feature in diabetic nephropathy, with loss of nephrin integrity con
300 critical mediator of vascular dysfunction in diabetic nephropathy, yet VEGF-A knockout and overexpres