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Journal articles on the topic 'Tubulointerstitial fibrosis'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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1

O'Donnell, Michael P. "Renal tubulointerstitial fibrosis." Postgraduate Medicine 108, no. 1 (July 2000): 159–72. http://dx.doi.org/10.3810/pgm.2000.07.1155.

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2

Zeisberg, Michael, and Eric G. Neilson. "Mechanisms of Tubulointerstitial Fibrosis." Journal of the American Society of Nephrology 21, no. 11 (September 23, 2010): 1819–34. http://dx.doi.org/10.1681/asn.2010080793.

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3

Kuncio, Gerald S., Eric G. Neilson, and Thomas Haverty. "Mechanisms of tubulointerstitial fibrosis." Kidney International 39, no. 3 (March 1991): 550–56. http://dx.doi.org/10.1038/ki.1991.63.

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Iwano, Masayuki, and Eric G. Neilson. "Mechanisms of tubulointerstitial fibrosis." Current Opinion in Nephrology and Hypertension 13, no. 3 (May 2004): 279–84. http://dx.doi.org/10.1097/00041552-200405000-00003.

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VIELHAUER, VOLKER, HANS-JOACHIM ANDERS, MATTHIAS MACK, JOSEF CIHAK, FRANK STRUTZ, MANFRED STANGASSINGER, BRUNO LUCKOW, HERMANN-JOSEF GRÖNE, and DETLEF SCHLÖNDORFF. "Obstructive Nephropathy in the Mouse: Progressive Fibrosis Correlates with Tubulointerstitial Chemokine Expression and Accumulation of CC Chemokine Receptor 2- and 5-Positive Leukocytes." Journal of the American Society of Nephrology 12, no. 6 (June 2001): 1173–87. http://dx.doi.org/10.1681/asn.v1261173.

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Abstract. The infiltration of leukocytes plays a major role in mediating tubulointerstitial inflammation and fibrosis in chronic renal disease. CC chemokines participate in leukocyte migration and infiltration into inflamed renal tissue. Because CC chemokine-directed leukocyte migration is mediated by target cell expression of a group of CC chemokine receptors, this study examined the expression of CC chemokines and their receptors during initiation of tubulointerstitial fibrosis after unilateral ureteral obstruction in C57BL/6 mice. Obstructed kidneys developed hydronephrosis, tubular cell da

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Thomas, S. E., S. Anderson, K. L. Gordon, T. T. Oyama, S. J. Shankland, and R. J. Johnson. "Tubulointerstitial disease in aging: evidence for underlying peritubular capillary damage, a potential role for renal ischemia." Journal of the American Society of Nephrology 9, no. 2 (February 1998): 231–42. http://dx.doi.org/10.1681/asn.v92231.

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Aging is associated with a progressive decline in renal function and the development of glomerulosclerosis and interstitial fibrosis. Although many studies have addressed the cellular mechanisms of age-related glomerulosclerosis, less is known about the tubulointerstitial fibrosis. In this study, aging (24 mo) rats develop tubulointerstitial fibrosis characterized by tubular injury and focal tubular cell proliferation, myofibroblast activation, macrophage infiltration with increased immunostaining for the adhesive proteins osteopontin and intercellular adhesion molecule-1, and collagen IV depo

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Ito, Hideyuki, Xiaoxiang Yan, Nanae Nagata, Kosuke Aritake, Yoshinori Katsumata, Tomohiro Matsuhashi, Masataka Nakamura, et al. "PGD2-CRTH2 Pathway Promotes Tubulointerstitial Fibrosis." Journal of the American Society of Nephrology 23, no. 11 (September 20, 2012): 1797–809. http://dx.doi.org/10.1681/asn.2012020126.

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Boor, Peter, Andrzej Konieczny, Luigi Villa, Anna-Lisa Schult, Eva Bücher, Song Rong, Uta Kunter, et al. "Complement C5 Mediates Experimental Tubulointerstitial Fibrosis." Journal of the American Society of Nephrology 18, no. 5 (March 27, 2007): 1508–15. http://dx.doi.org/10.1681/asn.2006121343.

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Sakamoto, Izumi, Yasuhiko Ito, Masashi Mizuno, Yasuhiro Suzuki, Akiho Sawai, Akio Tanaka, Shoichi Maruyama, Yoshifumi Takei, Yukio Yuzawa, and Seiichi Matsuo. "Lymphatic vessels develop during tubulointerstitial fibrosis." Kidney International 75, no. 8 (April 2009): 828–38. http://dx.doi.org/10.1038/ki.2008.661.

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10

SATOH, MINORU, NAOKI KASHIHARA, YASUSHI YAMASAKI, KEISUKE MARUYAMA, KAZUNORI OKAMOTO, YOUHEI MAESHIMA, HITOSHI SUGIYAMA, TAKESHI SUGAYA, KAZUO MURAKAMI, and HIROFUMI MAKINO. "Renal Interstitial Fibrosis Is Reduced in Angiotensin II Type 1a Receptor-Deficient Mice." Journal of the American Society of Nephrology 12, no. 2 (February 2001): 317–25. http://dx.doi.org/10.1681/asn.v122317.

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Abstract. Unilateral ureteral obstruction (UUO) results in tubulointerstitial fibrosis of the affected kidney by stimulating the renin-angiotensin system. This study established a UUO model in angiotensin type 1a receptor (AT1a) deficient (mutant) mice to elucidate the role of angiotensin II through AT1a on the fibrosis of the obstructed kidney (OBK). The relative volume of the tubulointerstitium was measured by an image analyzer; deposition of collagen types III and IV and monocyte/macrophage infiltration were histologically examined using specific antibodies. Also determined were the mRNA le

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11

Hewitson, Tim D. "Renal tubulointerstitial fibrosis: common but never simple." American Journal of Physiology-Renal Physiology 296, no. 6 (June 2009): F1239—F1244. http://dx.doi.org/10.1152/ajprenal.90521.2008.

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Regardless of etiology, all patients with chronic renal disease show a progressive decline in renal function with time. Fibrosis, so-called scarring, is a key cause of this pathophysiology. Fibrosis involves an excess accumulation of extracellular matrix (primarily composed of collagen) and usually results in loss of function when normal tissue is replaced with scar tissue. While recent major advances have led to a much better understanding of this process, many problems remain. We for instance know little about why some wounds heal and others scar and little about how many putative antifibrot

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Wu, Jinhao, Chao Huang, Gang Kan, Hanyu Xiao, Xiaoping Zhang та Jun Yang. "Silymarin Regulates Tgf-β1/Smad3 Signaling Pathway and Improves Renal Tubular Interstitial Fibrosis Caused by Obstructive Nephropathy". Current Topics in Nutraceutical Research 19, № 4 (17 березня 2021): 508–13. http://dx.doi.org/10.37290/ctnr2641-452x.19:508-513.

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Obstructive nephropathy often leads to renal tubulointerstitial fibrosis. Understanding of the pathogenesis of renal tubulointerstitial fibrosis caused by obstructive nephropathy is crucial to the development of effective therapeutic drugs to improve the prognosis of the patients. Silymarin, a polyphenolic flavonoid extracted from plants, has been shown to exhibit antiinflammatory and antioxidant effects ameliorating liver and kidney damage. However, the effect of silymarin on renal fibrosis in obstructive nephropathy remains to be explored. In this study, we found silymarin improved interstit

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13

Gewin, Leslie, та Roy Zent. "How Does TGF-β Mediate Tubulointerstitial Fibrosis?" Seminars in Nephrology 32, № 3 (травень 2012): 228–35. http://dx.doi.org/10.1016/j.semnephrol.2012.04.001.

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14

Li, Dixin, Hongbing Zeng, and Chunyang Ji. "Effect of pirfenidone on renal tubulointerstitial fibrosis." Frontiers of Medicine in China 3, no. 3 (July 10, 2009): 316–22. http://dx.doi.org/10.1007/s11684-009-0045-2.

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15

Johnson, Richard J., Christian Hugo, Leah Haseley, Raimund Pichler, James Bassuk, Susan Thomas, Shinichi Suga, William G. Couser, and Stuart J. Shankland. "Mechanisms of progressive glomerulosclerosis and tubulointerstitial fibrosis." Clinical and Experimental Nephrology 2, no. 4 (December 1998): 307–12. http://dx.doi.org/10.1007/bf02480459.

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16

Kümpers, Philipp, Faikah Gueler, Song Rong, Michael Mengel, Irini Tossidou, Imke Peters, Hermann Haller та Mario Schiffer. "Leptin is a coactivator of TGF-β in unilateral ureteral obstructive kidney disease". American Journal of Physiology-Renal Physiology 293, № 4 (жовтень 2007): F1355—F1362. http://dx.doi.org/10.1152/ajprenal.00003.2007.

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Progressive tubulointerstitial fibrosis is the common end point leading to end-stage renal disease in experimental and clinical settings. Since the peptide hormone leptin is involved not only in the regulation of obesity but also in the regulation of inflammation and fibrosis, we tested the hypothesis whether leptin deficiency has an impact on tubulointerstitial fibrosis in mice. Leptin-deficient ( ob/ ob) and leptin receptor-deficient mice ( db/ db) were exposed to 14 days of unilateral ureteral obstruction (UUO). The degree of fibrosis and inflammation was compared with that in sham-operated

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Wei, Jinying, Xinna Deng, Yang Li, Runmei Li, Zhaohua Yang, Xiuyuan Li, Shan Song, Yonghong Shi, Huijun Duan та Haijiang Wu. "PP2 Ameliorates Renal Fibrosis by Regulating the NF-κB/COX-2 and PPARγ/UCP2 Pathway in Diabetic Mice". Oxidative Medicine and Cellular Longevity 2021 (17 вересня 2021): 1–24. http://dx.doi.org/10.1155/2021/7394344.

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Renal fibrosis is characterized by glomerulosclerosis and tubulointerstitial fibrosis in diabetic nephropathy (DN). We aimed to evaluate the effects of PP2 on renal fibrosis of DN. GSE33744 and GSE86300 were downloaded from the GEO database. Firstly, 839 DEGs were identified between nondiabetic and diabetic mice renal glomerular samples. COX-2 was selected to assess the effects of PP2 on renal glomerulosclerosis. In db/db mice, PP2 decreased the expression of COX-2, phosphorylated p65, and fibrotic proteins, accompanied with attenuated renal glomerulosclerosis. In cultured glomerular mesangial

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Hruska, Keith A., Guangjie Guo, Magdalena Wozniak, Daniel Martin, Steven Miller, Helen Liapis, Kenneth Loveday, Saulo Klahr, T. Kuber Sampath, and Jeremiah Morrissey. "Osteogenic protein-1 prevents renal fibrogenesis associated with ureteral obstruction." American Journal of Physiology-Renal Physiology 279, no. 1 (July 1, 2000): F130—F143. http://dx.doi.org/10.1152/ajprenal.2000.279.1.f130.

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Unilateral ureteral obstruction (UUO) is a model of renal injury characterized by progressive tubulointerstitial fibrosis and renal damage, while relatively sparing the glomerulus and not producing hypertension or abnormalities in lipid metabolism. Tubulointerstitial fibrosis is a major component of several kidney diseases associated with the progression to end-stage renal failure. Here we report that when a critical renal developmental morphogen, osteogenic protein-1 (OP-1; 100 or 300 μg/kg body wt), is administered at the time of UUO and every other day thereafter, interstitial inflammation

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Nasu, Kahori, Takahisa Kawakami, Akinari Shinohara, Takeharu Sakamoto, and Masaomi Nangaku. "Munc18-1-interacting protein 3 mitigates renal fibrosis through protection of tubular epithelial cells from apoptosis." Nephrology Dialysis Transplantation 35, no. 4 (September 8, 2019): 576–86. http://dx.doi.org/10.1093/ndt/gfz177.

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Abstract Background Tubulointerstitial fibrosis is a hallmark of chronic kidney disease (CKD), and is initiated by tubular epithelial cell (TEC) injury. Hypoxia promotes tubular cell death, fibrosis and CKD progression. Munc18-1-interacting protein 3 (Mint3) is a molecule that activates hypoxia-inducible factors (HIFs) by binding and suppressing factor inhibiting HIF-1 (FIH). However, the role of Mint3 in tubulointerstitial fibrosis remains unknown. Methods We induced fibrosis of the kidney after unilateral ischemia–reperfusion injury (uIRI) in Mint3-knockout and littermate wild-type mice. The

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Mukhtarova, A. V., M. M. Batyushin, Е. А. Sinelnik, and N. V. Antipova. "Role of MCP-1 in the development of tubulointerstitial fibrosis in patients with primary chronic glomerulonephritis." Nephrology (Saint-Petersburg) 25, no. 5 (September 2, 2021): 92–98. http://dx.doi.org/10.36485/1561-6274-2021-25-5-92-98.

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BACKGROUND. To date, the study of the factors involved in the glomerular-tubular pathological connections leading to damage to the tubulointerstitial tissue is one of the topical areas of nephrology. THE AIM: to study the effect of MCP-1 in the development of tubulointerstitial fibrosis as a factor in the irreversible progression of chronic renal failure. PATIENTS ANDMETHODS. Prospective observation and retrospective analysis of case histories were carried out, which included a total of 75 patients with primary chronic glomerulonephritis. RESULTS. The average age of the patients was 36.7 ± 12.

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Schanstra, Joost, Johan Duchene, Laurence Desmond, Eric Neau, Denis Calise, Serge Estaque, Jean-Pierre Girolami, and Jean-Loup Bascands. "The protective effect of angiotensin converting enzyme inhibition in experimental renal fibrosis in mice is not mediated by bradykinin B2 receptor activation." Thrombosis and Haemostasis 89, no. 04 (2003): 735–40. http://dx.doi.org/10.1055/s-0037-1613580.

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SummaryUnilateral ureteral obstruction (UUO) is an animal model of accelerated renal tubulointerstitial fibrosis. We have recently shown, using this model, that mice lacking the bradykinin B2-receptor (B2-/- ) were more susceptible than control animals to the development of tubulointerstitial fibrosis. Angiotensin converting enzyme (ACE) inhibition slows down UUO-induced renal fibrosis. Since ACE-inhibition increases bradykinin and decreases angiotensin II concentrations we have verified if bradykinin is involved in the antifibrotic effects of ACE-inhibition using the UUO-model and B2-/- mice.

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22

Wang, Bin, Wei Ding, Minmin Zhang, Hongmei Li, and Yong Gu. "Rapamycin Attenuates Aldosterone-Induced Tubulointerstitial Inflammation and Fibrosis." Cellular Physiology and Biochemistry 35, no. 1 (2015): 116–25. http://dx.doi.org/10.1159/000369680.

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Background/Aim: Aldosterone (Aldo), a mediator of kidney fibrosis, is implicated in the pathogenesis of chronic kidney diseases (CKD). The aim of this study was to evaluate the regulatory role of rapamycin (Rap) in Aldo-induced tubulointerstitial inflammation and fibrosis. Methods: Uninephrectomized, Sprague-Dawley rats were given 1% NaCl (salt) to drink and were randomized to receive treatment for 28 days as follows: vehicle infusion (control), 0.75 μg/h Aldo subcutaneous infusion, or Aldo infusion plus 1 mg/kg/day of Rap by intraperitoneal injection. The effect of Rap on Aldo-induced fibrosi

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Peng, Wen, Jie Zhao, Li Wang, Aili Cao, Minqian Jiang, and Xia Chen. "Renal Tubulointerstitial Fibrosis: A Review in Animal Models." Journal of Integrative Nephrology and Andrology 2, no. 3 (2015): 75. http://dx.doi.org/10.4103/2225-1243.161428.

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Strutz, Frank. "Pathogenesis of tubulointerstitial fibrosis in chronic allograft dysfunction." Clinical Transplantation 23 (December 2009): 26–32. http://dx.doi.org/10.1111/j.1399-0012.2009.01106.x.

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JUNGTHIRAPANICH, Jaakchai, Vararat SINGKHWA, Dhevy WATANA, Prasit FUTRAKUL, Rachanee SENSIRIVATANA, and Saowanee YENRUDI. "Significance of tubulointerstitial fibrosis in paediatric IgM nephropathy." Nephrology 3, no. 4 (August 1997): 509–14. http://dx.doi.org/10.1111/j.1440-1797.1997.tb00234.x.

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26

Sato, Norihiro, Kazumi Shiraiwa, Kiyonori Kai, Atsushi Watanabe, Shinichi Ogawa, Yoshiro Kobayashi, Hiroko Yamagishi-Imai, Yasunori Utsunomiya, and Tetsuya Mitarai. "Mizoribine Ameliorates the Tubulointerstitial Fibrosis of Obstructive Nephropathy." Nephron 89, no. 2 (2001): 177–85. http://dx.doi.org/10.1159/000046065.

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Hebiguchi, Tatsuzo, Tetsuo Kato, Hiroaki Yoshino, Masaru Mizuno, Hideki Wakui, Atsushi Komatsuda, and Hirokazu Imai. "Extremely Short Small Bowel Induces Focal Tubulointerstitial Fibrosis." Journal of Pediatric Gastroenterology and Nutrition 32, no. 5 (May 2001): 586–92. http://dx.doi.org/10.1097/00005176-200105000-00018.

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Oba, Shigeyoshi, Shintaro Kumano, Etsu Suzuki, Hiroaki Nishimatsu, Masao Takahashi, Hajime Takamori, Masatoshi Kasuya, et al. "miR-200b Precursor Can Ameliorate Renal Tubulointerstitial Fibrosis." PLoS ONE 5, no. 10 (October 25, 2010): e13614. http://dx.doi.org/10.1371/journal.pone.0013614.

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Burns, Kevin D. "Interleukin-1β as a mediator of tubulointerstitial fibrosis". Kidney International 62, № 1 (липень 2002): 346–47. http://dx.doi.org/10.1046/j.1523-1755.2002.00439.x.

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30

Qi, Weier, Xinming Chen, Philip Poronnik, and Carol A. Pollock. "The renal cortical fibroblast in renal tubulointerstitial fibrosis." International Journal of Biochemistry & Cell Biology 38, no. 1 (January 2006): 1–5. http://dx.doi.org/10.1016/j.biocel.2005.09.005.

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Chen, Tso-Hsiao, Yuh-Mou Sue, Chung-Yi Cheng, and Cheng-Hsien Chen. "MP061FUCOXANTHIN REDUCES RENAL TUBULOINTERSTITIAL FIBROSIS BY UPREGULATING NHE1." Nephrology Dialysis Transplantation 32, suppl_3 (May 1, 2017): iii448. http://dx.doi.org/10.1093/ndt/gfx162.mp061.

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Pak, Eun Seon, Lak Shin Jeong, Xiyan Hou, Sushil K. Tripathi, Jiyoun Lee, and Hunjoo Ha. "Dual Actions of A2A and A3 Adenosine Receptor Ligand Prevents Obstruction-Induced Kidney Fibrosis in Mice." International Journal of Molecular Sciences 22, no. 11 (May 26, 2021): 5667. http://dx.doi.org/10.3390/ijms22115667.

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Kidney fibrosis is the final outcome of chronic kidney disease (CKD). Adenosine plays a significant role in protection against cellular damage by activating four subtypes of adenosine receptors (ARs), A1AR, A2AAR, A2BAR, and A3AR. A2AAR agonists protect against inflammation, and A3AR antagonists effectively inhibit the formation of fibrosis. Here, we showed for the first time that LJ-4459, a newly synthesized dual-acting ligand that is an A2AAR agonist and an A3AR antagonist, prevents the progression of tubulointerstitial fibrosis. Unilateral ureteral obstruction (UUO) surgery was performed on

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Colon, Selene, Haiyan Luan, Yan Liu, Cameron Meyer, Leslie Gewin, and Gautam Bhave. "Peroxidasin and eosinophil peroxidase, but not myeloperoxidase, contribute to renal fibrosis in the murine unilateral ureteral obstruction model." American Journal of Physiology-Renal Physiology 316, no. 2 (February 1, 2019): F360—F371. http://dx.doi.org/10.1152/ajprenal.00291.2018.

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Renal fibrosis is the pathological hallmark of chronic kidney disease (CKD) and manifests as glomerulosclerosis and tubulointerstitial fibrosis. Reactive oxygen species contribute significantly to renal inflammation and fibrosis, but most research has focused on superoxide and hydrogen peroxide (H2O2). The animal heme peroxidases myeloperoxidase (MPO), eosinophil peroxidase (EPX), and peroxidasin (PXDN) uniquely metabolize H2O2 into highly reactive and destructive hypohalous acids, such as hypobromous and hypochlorous acid. However, the role of these peroxidases and their downstream hypohalous

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Wu, Weiju, Chengfei Liu, Conrad A. Farrar, Liang Ma, Xia Dong, Steven H. Sacks, Ke Li, and Wuding Zhou. "Collectin-11 Promotes the Development of Renal Tubulointerstitial Fibrosis." Journal of the American Society of Nephrology 29, no. 1 (November 15, 2017): 168–81. http://dx.doi.org/10.1681/asn.2017050544.

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Collectin-11 is a recently described soluble C-type lectin, a pattern recognition molecule of the innate immune system that has distinct roles in host defense, embryonic development, and acute inflammation. However, little is known regarding the role of collectin-11 in tissue fibrosis. Here, we investigated collectin-11 in the context of renal ischemia-reperfusion injury. Compared with wild-type littermate controls, Collec11 deficient (CL-11−/−) mice had significantly reduced renal functional impairment, tubular injury, renal leukocyte infiltration, renal tissue inflammation/fibrogenesis, and

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Hewitson, T. D., I. A. Darby, T. Bisucci, C. L. Jones, and G. J. Becker. "Evolution of tubulointerstitial fibrosis in experimental renal infection and scarring." Journal of the American Society of Nephrology 9, no. 4 (April 1998): 632–42. http://dx.doi.org/10.1681/asn.v94632.

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Renal tubulointerstitial fibrosis may result from a loss of tubulointerstitial volume, which produces a disproportionate increase in the density of matrix. This study examines the relationship between fibrogenesis and collapse in scar formation after experimental renal infection. Escherichia coli were inoculated into the renal cortex of Sprague Dawley rats, with saline substituted in a control group. Glomerular, tubular, and interstitial profile areas were determined. Density of glomerular profiles was used as a measure of tubulointerstitial collapse. Collagen type I, III, and IV expression wa

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KÖKSAL CEVHER, Şimal, Ezgi ÇOŞKUN YENİGÜN, Ramazan ÖZTÜRK, Didem TURGUT, Nihal ÖZKAYAR, Nergiz BAYRAKÇI, and Fatih DEDE. "A Rare Cause of Acute Tubulointerstitial Nephritis: Retroperitoneal Fibrosis: Case Report." Turkiye Klinikleri Journal of Internal Medicine 1, no. 2 (2016): 99–102. http://dx.doi.org/10.5336/intermed.2015-47087.

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An, Won Suk, Hyun Ju Kim, Kyu-Hyang Cho, and Nosratola D. Vaziri. "Omega-3 fatty acid supplementation attenuates oxidative stress, inflammation, and tubulointerstitial fibrosis in the remnant kidney." American Journal of Physiology-Renal Physiology 297, no. 4 (October 2009): F895—F903. http://dx.doi.org/10.1152/ajprenal.00217.2009.

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Significant reduction of renal mass initiates a series of hemodynamic and nonhemodynamic events which lead to proteinuria, glomerulosclerosis, tubulointerstitial injury, and end-stage renal failure. Lipid mediators derived from fatty acids participate in regulation of renal hemodynamic and nonhemodynamic processes that influence progression of renal disease. Composition of cellular fatty acids and hence related signaling responses are influenced by their dietary contents. Consumption of omega-3 fatty acids (O-3FA) has proven effective in mitigating atherosclerosis. We tested the hypothesis tha

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Hamar, Péter, and Dontscho Kerjaschki. "Blood capillary rarefaction and lymphatic capillary neoangiogenesis are key contributors to renal allograft fibrosis in an ACE inhibition rat model." American Journal of Physiology-Heart and Circulatory Physiology 311, no. 4 (October 1, 2016): H981—H990. http://dx.doi.org/10.1152/ajpheart.00320.2016.

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Chronic allograft fibrosis is the major cause of graft loss in kidney transplantation. Progression can only be reduced by inhibition of the renin-angiotensin system (RAS). We tested the hypothesis that the protection provided by angiotensin-converting enzyme (ACE) inhibition also decreases capillary rarefaction, lymphangiogenesis, and podocyte injury in allograft fibrosis. Fisher kidneys were transplanted into bilaterally nephrectomized Lewis rats treated with enalapril (60 mg/kg per day) (ACE inhibitor, ACEi) or vehicle. Proteinuria, blood urea nitrogen, and plasma creatinine were regularly a

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Tian, Shaojiang, Guohua Ding, Ruhan Jia, and Guili Chu. "Tubulointerstitial Macrophage Accumulation is Regulated by Sequentially Expressed Osteopontin and Macrophage Colony-Stimulating Factor: Implication for the Role of Atorvastatin." Mediators of Inflammation 2006 (2006): 1–9. http://dx.doi.org/10.1155/mi/2006/12919.

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Infiltration and local proliferation are known factors that contribute to tubulointerstitial macrophage accumulation. This study explored the time course of these two contributors' roles as tubulointerstitial inflammation and fibrosis progressing, and evaluated the mechanisms of the protective effect of atorvastatin. Unilateral ureteral obstructive (UUO) rats were treated with atorvastatin (10 mg/Kg) or vehicle. Expression of osteopontin (OPN) and macrophage colony-stimulating factor (M-CSF) was evaluated by RT-PCR and immunohistochemistry. Immunohistochemistry staining of ED1 was used to asse

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Maksimowski, Nicholas A., James W. Scholey, and Vanessa R. Williams. "Sex and kidney ACE2 expression in primary focal segmental glomerulosclerosis: A NEPTUNE study." PLOS ONE 16, no. 6 (June 7, 2021): e0252758. http://dx.doi.org/10.1371/journal.pone.0252758.

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Background Angiotensin-converting enzyme 2 (ACE2) has been implicated in the pathogenesis of experimental kidney disease. ACE2 is on the X chromosome, and in mice, deletion of ACE2 leads to the development of focal segmental glomerulosclerosis (FSGS). The relationship between sex and renal ACE2 expression in humans with kidney disease is a gap in current knowledge. Methods We studied renal tubulointerstitial microarray data and clinical variables from subjects with FSGS enrolled in the Nephrotic Syndrome Study Network (NEPTUNE) study. We compared relationships between ACE2 expression and age,

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Schaier, Matthias, Stefanie Vorwalder, Claudia Sommerer, Ralf Dikow, Friederike Hug, Marie-Luise Gross, Rüdiger Waldherr, and Martin Zeier. "Role of FTY720 on M1 and M2 macrophages, lymphocytes, and chemokines in \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \({5}/{6}\) \end{document} nephrectomized rats." American Journal of Physiology-Renal Physiology 297, no. 3 (September 2009): F769—F780. http://dx.doi.org/10.1152/ajprenal.90530.2008.

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Renal injury is accompanied by the presence of infiltrating inflammatory cells in the glomerulus and tubulointerstitium. FTY720 modifies lymphocyte migration into injured tissues by lymphocyte sequestration to secondary lymphoid organs. The purpose of this study was to examine the potential of FTY720 to influence the inflammatory response in a nonimmunological model of renal failure. Sham-operated and [Formula: see text] nephrectomized (SNX) Sprague-Dawley rats received two different doses of FTY720 or vehicle orally for 14 wk. Treatment with FTY720 reduced glomerular and tubulointerstitial da

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Jin, Jixiu, Tian Wang, Woong Park, Wenjia Li, Won Kim, Sung Kwang Park, and Kyung Pyo Kang. "Inhibition of Yes-Associated Protein by Verteporfin Ameliorates Unilateral Ureteral Obstruction-Induced Renal Tubulointerstitial Inflammation and Fibrosis." International Journal of Molecular Sciences 21, no. 21 (October 31, 2020): 8184. http://dx.doi.org/10.3390/ijms21218184.

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Yes-associated protein (YAP) activation after acute ischemic kidney injury might be related to interstitial fibrosis and impaired renal tubular regeneration. Verteporfin (VP) is a photosensitizer used in photodynamic therapy to treat age-related macular degeneration. In cancer cells, VP inhibits TEA domain family member (TEAD)-YAP interactions without light stimulation. The protective role of VP in unilateral ureteral obstruction (UUO)-induced renal fibrosis and related mechanisms remains unclear. In this study, we investigate the protective effects of VP on UUO-induced renal tubulointerstitia

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Guo, Honglei, Xiao Bi, Ping Zhou, Shijian Zhu, and Wei Ding. "NLRP3 Deficiency Attenuates Renal Fibrosis and Ameliorates Mitochondrial Dysfunction in a Mouse Unilateral Ureteral Obstruction Model of Chronic Kidney Disease." Mediators of Inflammation 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/8316560.

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Background and Aims. The nucleotide-binding domain and leucine-rich repeat containing PYD-3 (NLRP3) inflammasome has been implicated in the pathogenesis of chronic kidney disease (CKD); however, its exact role in glomerular injury and tubulointerstitial fibrosis is still undefined. The present study was performed to identify the function of NLRP3 in modulating renal injury and fibrosis and the potential involvement of mitochondrial dysfunction in the murine unilateral ureteral obstruction (UUO) model of CKD. Methods. Employing wild-type (WT) and NLRP3−/− mice with or without UUO, we evaluated

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You, Ran, Wei Zhou, Yanwei Li, Yue Zhang, Songming Huang, Zhanjun Jia, and Aihua Zhang. "Inhibition of ROCK2 alleviates renal fibrosis and the metabolic disorders in the proximal tubular epithelial cells." Clinical Science 134, no. 12 (June 2020): 1357–76. http://dx.doi.org/10.1042/cs20200030.

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Abstract Non-specific inhibition of Rho-associated kinases (ROCKs) alleviated renal fibrosis in the unilateral ureteral obstruction (UUO) model, while genetic deletion of ROCK1 did not affect renal pathology in mice. Thus, whether ROCK2 plays a role in renal tubulointerstitial fibrosis needs to be clarified. In the present study, a selective inhibitor against ROCK2 or genetic approach was used to investigate the role of ROCK2 in renal tubulointerstitial fibrosis. In the fibrotic kidneys of chronic kidney diseases (CKDs) patients, we observed an enhanced expression of ROCK2 with a positive corr

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Xavier, Sandhya, Ranjit K. Sahu, Susan G. Landes, Jing Yu, Ronald P. Taylor, Srinivas Ayyadevara, Judit Megyesi, et al. "Pericytes and immune cells contribute to complement activation in tubulointerstitial fibrosis." American Journal of Physiology-Renal Physiology 312, no. 3 (March 1, 2017): F516—F532. http://dx.doi.org/10.1152/ajprenal.00604.2016.

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We have examined the pathogenic role of increased complement expression and activation during kidney fibrosis. Here, we show that PDGFRβ-positive pericytes isolated from mice subjected to obstructive or folic acid injury secrete C1q. This was associated with increased production of proinflammatory cytokines, extracellular matrix components, collagens, and increased Wnt3a-mediated activation of Wnt/β-catenin signaling, which are hallmarks of myofibroblast activation. Real-time PCR, immunoblots, immunohistochemistry, and flow cytometry analysis performed in whole kidney tissue confirmed increase

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Vidyasagar, Aparna, Shannon Reese, Zeki Acun, Debra Hullett, and Arjang Djamali. "HSP27 is involved in the pathogenesis of kidney tubulointerstitial fibrosis." American Journal of Physiology-Renal Physiology 295, no. 3 (September 2008): F707—F716. http://dx.doi.org/10.1152/ajprenal.90240.2008.

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We hypothesized that heat shock protein 27 (HSP27), a small heat shock protein with actin-remodeling properties, is involved in the pathogenesis of kidney tubulointerstitial fibrosis. We first examined its expression in the rat unilateral ureteral obstruction (UUO) model of kidney fibrosis and epithelial-to-mesenchymal transition (EMT). Immunoblot analyses showed that UUO resulted in significant upregulation of TGF-β1, α-smooth muscle actin (α-SMA), total and phosphorylated HSP27, and phosphorylated p38MAPK. Immunofluorescence studies showed that HSP27 costained with TGF-β1, α-SMA, and E-cadhe

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Morrissey, J. J., S. Ishidoya, R. McCracken, and S. Klahr. "Nitric oxide generation ameliorates the tubulointerstitial fibrosis of obstructive nephropathy." Journal of the American Society of Nephrology 7, no. 10 (October 1996): 2202–12. http://dx.doi.org/10.1681/asn.v7102202.

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Angiotensin-converting enzyme (ACE) inhibitors have been shown to minimize fibrosis of the kidney tubulointerstitium in several diseases. In addition to lowering angiotensin II levels, ACE inhibitors can increase kinin levels and subsequently increase nitric oxide formation. To determine whether nitric oxide generation is a component of the beneficial effect of ACE inhibitors on renal fibrosis, enalapril, enalapril plus NG-nitro-L-arginine methyl ester (L-NAME) or L-arginine was administered to rats that had undergone unilateral ureteral obstruction (UUO). Ureteral obstruction caused significa

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Cina, Davide P., Hui Xu, Limin Liu, Laszlo Farkas, Daniela Farkas, Martin Kolb, and Peter J. Margetts. "Renal tubular angiogenic dysregulation in anti-Thy1.1 glomerulonephritis." American Journal of Physiology-Renal Physiology 300, no. 2 (February 2011): F488—F498. http://dx.doi.org/10.1152/ajprenal.00214.2010.

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Peritubular vascular changes and hypoxia after glomerular injury may explain subsequent tubulointerstitial injury and fibrosis. Several studies suggested that the expected tubulointerstitial angiogenic response is actively suppressed in this setting. The mechanism of this aberrant response has not been clearly identified. We used a common model of glomerular injury in rats to assess vascular changes and to identify potential factors associated with this aberrant response. Anti-Thy1.1 antibody administration (1 or 4 weekly doses) led to a dose-dependent renal damage characterized by elevated ur

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Ma, Ze-jun, Xiao-na Zhang, Li Li, Wei Yang, Shan-shan Wang, Xin Guo, Pei Sun, and Li-ming Chen. "Tripterygium Glycosides Tablet Ameliorates Renal Tubulointerstitial Fibrosis via the Toll-Like Receptor 4/Nuclear Factor Kappa B Signaling Pathway in High-Fat Diet Fed and Streptozotocin-Induced Diabetic Rats." Journal of Diabetes Research 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/390428.

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Tripterygium glycosides tablet (TGT) is a Chinese traditional medicine that has been shown to protect podocytes from injury and reduce the proteinuria. The aim of this study was to assess the effect of TGT on renal tubulointerstitial fibrosis and its potential mechanism in high-fat diet fed and STZ-induced diabetic rats. Rats were randomly divided into normal control rats (NC group), diabetic rats without drug treatment (DM group), and diabetic rats treated with TGT (1, 3, or 6 mg/kg/day, respectively) for 8 weeks. The results showed that 24 h proteinuria and urinary N-acetyl-glucosaminidase (

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Prakash, Jai, Klaas Poelstra, Harry Goor, Frits Moolenaar, Dirk Meijer, and Robbert Kok. "Novel Therapeutic Targets for the Treatment of Tubulointerstitial Fibrosis." Current Signal Transduction Therapy 3, no. 2 (May 1, 2008): 97–111. http://dx.doi.org/10.2174/157436208784223161.

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