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| 001 | 137573 | ||
| 005 | 20240229111724.0 | ||
| 024 | 7 | _ | |a 10.1016/j.kint.2018.06.006 |2 doi |
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| 041 | _ | _ | |a eng |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Micakovic, Tamara |b 0 |
| 245 | _ | _ | |a The angiotensin II type 2 receptors protect renal tubule mitochondria in early stages of diabetes mellitus. |
| 260 | _ | _ | |a Basingstoke |c 2018 |b Nature Publishing Group |
| 336 | 7 | _ | |a article |2 DRIVER |
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| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a Diabetic nephropathy correlates more closely to defective mitochondria and increased oxidative stress in the kidney than to hyperglycemia. A key driving factor of diabetic nephropathy is angiotensin II acting via the G-protein-coupled cell membrane type 1 receptor. The present study aimed to investigate the role of the angiotensin II type 2 receptor (AT2R) at the early stages of diabetic nephropathy. Using receptor binding studies and immunohistochemistry we found that the mitochondria in renal tubules contain high-affinity AT2Rs. Increased renal mitochondrial AT2R density by transgenic overexpression was associated with reduced superoxide production of isolated mitochondria from non-diabetic rats. Streptozotocin-induced diabetes (28 days) caused a drop in the ATP/oxygen ratio and an increase in the superoxide production of isolated renal mitochondria from wild-type diabetic rats. This correlated with changes in the renal expression profile and increased tubular epithelial cell proliferation. AT2R overexpression in tubular epithelial cells inhibited all diabetes-induced renal changes including a drop in mitochondrial bioenergetics efficiency, a rise in mitochondrial superoxide production, metabolic reprogramming, and increased proliferation. Thus, AT2Rs translocate to mitochondria and can contribute to reno-protective effects at early stages of diabetes. Hence, targeted AT2R overexpression in renal cells may open new avenues to develop novel types of drugs preventing diabetic nephropathy. |
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| 700 | 1 | _ | |a Papagiannarou, Stamatia |b 1 |
| 700 | 1 | _ | |a Clark, Euan |b 2 |
| 700 | 1 | _ | |a Kuzay, Yalcin |b 3 |
| 700 | 1 | _ | |a Abramovic, Katarina |b 4 |
| 700 | 1 | _ | |a Peters, Jörg |b 5 |
| 700 | 1 | _ | |a Sticht, Carsten |b 6 |
| 700 | 1 | _ | |a Volk, Nadine |b 7 |
| 700 | 1 | _ | |a Fleming, Thomas |b 8 |
| 700 | 1 | _ | |a Nawroth, Peter |b 9 |
| 700 | 1 | _ | |a Hammes, Hans-Peter |b 10 |
| 700 | 1 | _ | |a Alenina, Natalia |b 11 |
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| 700 | 1 | _ | |a Hoffmann, Sigrid Christa |b 13 |
| 773 | _ | _ | |a 10.1016/j.kint.2018.06.006 |g p. S0085253818304423 |0 PERI:(DE-600)2007940-0 |n 5 |p 937-950 |t Kidney international |v 94 |y 2018 |x 0085-2538 |
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| 910 | 1 | _ | |a Deutsches Krebsforschungszentrum |0 I:(DE-588b)2036810-0 |k DKFZ |b 12 |6 P:(DE-He78)00a2ea610aee4a8fca32908fc3d02e91 |
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