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1 elial PHD2, the main oxygen sensor, provided renoprotection.
2 ent with metformin, did not provide complete renoprotection.
3 tion similarly abolishes PGC1alpha-dependent renoprotection.
4 es DKD injury and abrogates the ATG-mediated renoprotection.
5 nd their dual action seems to confer greater renoprotection.
6 tially viable mechanism for AFSC-EV mediated renoprotection.
7 minuria, implying that canagliflozin confers renoprotection.
8 ING deletion in diabetic mice showed similar renoprotection.
9  receptor agonists, which confer significant renoprotection.
10 the pathways involved in their mechanisms of renoprotection.
11 e AFSC could be responsible for the observed renoprotection.
12 ith a single dose of UA afforded significant renoprotection against ischemic injury.
13 epresents a potential therapeutic target for renoprotection and prevention of fibrosis following acut
14 ial to signal injury and afford postischemic renoprotection and repair remains obscure.
15 n angiotensin-converting enzyme inhibitor on renoprotection and survival in 250 patients with hyperte
16 ent studies have not detected differences in renoprotection between ARB and ACEI.
17 ce, recent clinical trials have demonstrated renoprotection by angiotensin II inhibition in patients
18 ta demonstrating the physiologic evidence of renoprotection by antihypertensive therapy.
19          However, vitamin D may also promote renoprotection by suppressing renin transcription throug
20 a-globin gene locus in SSA patients confers "renoprotection" by mechanisms not related to the degree
21  animal models of chronic renal injury, such renoprotection can virtually eliminate progression of th
22 ult, suggesting that the previously reported renoprotection conferred by MSU likely results from exoc
23 r an S1P(1)R antagonist, suggesting that the renoprotection conferred by S1P(2)R antagonism results f
24  endogenous mediator of EPC mobilization and renoprotection, consistent with its novel function in ph
25 ation/transplantation, and suggest that this renoprotection correlates with decreased membrane lipid
26 mia-reperfusion injury and suggest that this renoprotection correlates with late vasodilatory prostan
27                                         This renoprotection corresponded with increases in cytoprotec
28                                The extent of renoprotection, decrease in cellular p53 and attenuation
29                                 Whether this renoprotection derives from a reduction of macrophages a
30 icity, which can be effectively targeted for renoprotection during chemotherapy.
31 geting PKCdelta as an effective strategy for renoprotection during cisplatin-based cancer therapy.
32                                 MitoQ showed renoprotection equivalent to ramipril but no synergistic
33     The role of lipid-lowering treatments in renoprotection for patients with diabetes is debated.
34         In humans with chronic renal injury, renoprotection has been successfully demonstrated only l
35 volved are largely unknown, and HIF-mediated renoprotection has not been examined in other causes of
36 y, xenon provided morphologic and functional renoprotection; hydrodynamic injection of HIF-1alpha sma
37 uding maximal ACE inhibition affords greater renoprotection in diabetic nephropathy despite a similar
38   However, whether ATG specifically provides renoprotection in DKD is not known.
39 inferior to enalapril in providing long-term renoprotection in persons with type 2 diabetes.
40  profile using juniper oil (JO) would afford renoprotection in rats treated with tacrolimus.
41 r injury may be reversible, the HIF-mediated renoprotection in VHL-KO mice was associated with activa
42 s of 5 days each month for 3 months promoted renoprotection, including reduction of proteinuria and i
43 nsin receptor blockers achieves only partial renoprotection, increasing the need for novel therapeuti
44                                 Whether this renoprotection involves enhanced GLP-1 signaling is uncl
45                                  Conversely, renoprotection is conferred by processes that upregulate
46                    Interest in pharmacologic renoprotection is currently directed toward statins and
47 n D signaling in podocytes accounts for this renoprotection is unknown.
48 ieved appears to be the major determinant of renoprotection, not the class of drug used.
49 onstrated for the first time that Xe confers renoprotection on renal grafts ex vivo and is likely to
50 , and there is uncertainty about the greater renoprotection seen in non-diabetic renal disease.
51 in this model, OMA affords greater long-term renoprotection than ENA when doses are adjusted to yield
52 he factors mediating possible ferric citrate renoprotection, the mechanisms by which they may act, an
53 sartan conferred similar (i.e., noninferior) renoprotection to 10 to 20 mg of enalapril as determined
54                                              Renoprotection was also consistent across studies irresp
55                           In Model 1 maximal renoprotection was demonstrated with the 6 mg/kg dose of