2013
DOI: 10.2337/db13-0135
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Abstract: The Ca2+-activated K+ channel KCa3.1 mediates cellular signaling processes associated with dysfunction of vasculature. However, the role of KCa3.1 in diabetic nephropathy is unknown. We sought to assess whether KCa3.1 mediates the development of renal fibrosis in two animal models of diabetic nephropathy. Wild-type and KCa3.1−/− mice, and secondly eNOS−/− mice, had diabetes induced with streptozotocin and then were treated with/without a selective inhibitor of KCa3.1 (TRAM34). Our results show that the albumin… Show more

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Cited by 81 publications
(94 citation statements)
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“…Positive signals in immunofluorescence were qualified as previous described [24]. It was found that the OPN group could decrease and the anti-OPN group could increase the formation of autophagosomes compared with the control group and the isotype control group, respectively, as demonstrated by immunofluorescence and co-focusing experimental analysis (Fig.…”
Section: Resultsmentioning
confidence: 97%
“…Positive signals in immunofluorescence were qualified as previous described [24]. It was found that the OPN group could decrease and the anti-OPN group could increase the formation of autophagosomes compared with the control group and the isotype control group, respectively, as demonstrated by immunofluorescence and co-focusing experimental analysis (Fig.…”
Section: Resultsmentioning
confidence: 97%
“…We have previously described that this animal model develops renal dysfunction and diabetes-induced tubulointerstitial injury. 28,29 The formation of autophagosomes was determined by LC3 expression, which participates in the initiation and elongation processes of autophagosomes, using indirect immunofluorescence staining. As shown in Figure 1, there is basal expression of LC3 in the kidneys of normal animals, which was increased in the diabetic mice (Po0.05).…”
Section: Resultsmentioning
confidence: 99%
“…After experimental myocardial infarction in rats, K Ca 3.1 expressions are increased in vascular cells, mononuclear cells, and fibroblasts in an infarction area [30]. Blockade of K Ca 3.1 channels can reduce asthma airway inflammation and ameliorate renal fibrosis [8,19]. Damage of K Ca 3.1 channel activation leads to T cell activation defects [18].…”
Section: Discussionmentioning
confidence: 98%
“…Genetic disruption of K Ca 3.1 or pharmacological blockade of K Ca 3.1 with TRAM-34 significantly reduced renal fibrosis in mice and rats following unilateral ureteral obstruction [14]. A recent study provides evidence that K Ca 3.1 mediates renal fibrosis in diabetic nephropathy through the TGF-β1/ Smad signaling pathway [19]. However, the contribution of K Ca 3.1 channels in cardiac fibrosis remains to be determined.…”
Section: Introductionmentioning
confidence: 97%