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Artykuły w czasopismach na temat „Tubular-interstitial fibrosis”

Autor: Grafiati

Data publikacji: 19 października 2024

Data aktualizacji: 31 lipca 2025

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1

Wyczanska, Maja, Jana Rohling, Ursula Keller, Marcus R. Benz, Carsten Kirschning, and Bärbel Lange-Sperandio. "TLR2 mediates renal apoptosis in neonatal mice subjected experimentally to obstructive nephropathy." PLOS ONE 18, no. 11 (2023): e0294142. http://dx.doi.org/10.1371/journal.pone.0294142.

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Urinary tract obstruction during renal development leads to inflammation, tubular apoptosis, and interstitial fibrosis. Toll like receptors (TLRs) expressed on leukocytes, myofibroblasts and renal cells play a central role in acute inflammation. TLR2 is activated by endogenous danger signals in the kidney; its contribution to renal injury in early life is still a controversial topic. We analyzed TLR2 for a potential role in the neonatal mouse model of congenital obstructive nephropathy. Inborn obstructive nephropathies are a leading cause of end-stage kidney disease in children. Thus, newborn

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Rascio, Federica, Paola Pontrelli, Giuseppe Stefano Netti, et al. "IgE-Mediated Immune Response and Antibody-Mediated Rejection." Clinical Journal of the American Society of Nephrology 15, no. 10 (2020): 1474–83. http://dx.doi.org/10.2215/cjn.02870320.

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Background and objectivesActive antibody-mediated rejection is the main cause of kidney transplant loss, sharing with SLE the alloimmune response and the systemic activation of the IFN-α pathway. IgE-mediated immune response plays a key role in the development of SLE nephritis and is associated with IFN-α secretion. The aim of our study was to investigate IgE-mediated immune response in antibody-mediated rejection.Design, setting, participants, & measurementsThis was a cross-sectional study of 56 biopsy-proven antibody-mediated rejection study participants, 80 recipients with normal graft

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3

Christensen, Erik I., and Pierre J. Verroust. "Interstitial fibrosis: tubular hypothesis versus glomerular hypothesis." Kidney International 74, no. 10 (2008): 1233–36. http://dx.doi.org/10.1038/ki.2008.421.

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Eskild-Jensen, Anni, Lene Fogt Paulsen, Lise Wogensen, et al. "AT1 receptor blockade prevents interstitial and glomerular apoptosis but not fibrosis in pigs with neonatal induced partial unilateral ureteral obstruction." American Journal of Physiology-Renal Physiology 292, no. 6 (2007): F1771—F1781. http://dx.doi.org/10.1152/ajprenal.00479.2006.

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Obstruction-induced fibrosis is a leading cause of end-stage renal failure in children. The pathophysiological mechanisms may involve apoptosis and the renin-angiotensin system. We studied apoptosis and fibrosis in a well-established neonatal pig model with unilateral partial ureteral obstruction (PUUO) induced during ongoing nephrogenesis in 2-day-old piglets. The role of angiotensin II (ANG II) was studied using the AT1 receptor blocker CV-11974 (0.12 mg/h candesartan from age 23 to 30 days). At day 30 the kidneys were perfusion fixed and fibrosis, apoptosis, and tubular lengths were quantit

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5

Wang, Shi-Nong, and Raimund Hirschberg. "Growth factor ultrafiltration in experimental diabetic nephropathy contributes to interstitial fibrosis." American Journal of Physiology-Renal Physiology 278, no. 4 (2000): F554—F560. http://dx.doi.org/10.1152/ajprenal.2000.278.4.f554.

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Glomerular proteinuria is a risk factor for progression of chronic renal failure and contributes to renal interstitial fibrosis. In experimental diabetic glomerular sclerosis, there is translocation of high-molecular-weight growth factors, namely, hepatocyte growth factor (HGF) and transforming growth factor (TGF)-β, from plasma into tubular fluid, both of which act on tubular cells through apical membrane receptors. In the present studies, the hypothesis is examined that ultrafiltered HGF and TGF-β induce increased expression of extracellular matrix (ECM) proteins directly in tubular cells, o

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6

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 (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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7

Leong, Khai Gene, Elyce Ozols, John Kanellis, David J. Nikolic-Paterson, and Frank Y. Ma. "Cyclophilin A Promotes Inflammation in Acute Kidney Injury but Not in Renal Fibrosis." International Journal of Molecular Sciences 21, no. 10 (2020): 3667. http://dx.doi.org/10.3390/ijms21103667.

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Cyclophilin A (CypA) is a highly abundant protein in the cytoplasm of most mammalian cells. Beyond its homeostatic role in protein folding, CypA is a Damage-Associated Molecular Pattern which can promote inflammation during tissue injury. However, the role of CypA in kidney disease is largely unknown. This study investigates the contribution of CypA in two different types of kidney injury: acute tubular necrosis and progressive interstitial fibrosis. CypA (Ppia) gene deficient and wild type (WT) littermate controls underwent bilateral renal ischaemia/reperfusion injury (IRI) and were killed 24

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8

Wang, Shudan, Ming Wu, Luis Chiriboga, Chaim Putterman, Anna Broder, and H. Michael Belmont. "4336 Renal Tubular Complement C9 Deposition is Associated with Renal Tubular Damage and Fibrosis in Lupus Nephritis." Journal of Clinical and Translational Science 4, s1 (2020): 144. http://dx.doi.org/10.1017/cts.2020.424.

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OBJECTIVES/GOALS: Tubulointerstitial damage in lupus nephritis (LN) is a strong predictor of progression to chronic kidney disease and end stage renal disease (ESRD). While complement activation mediates glomerular injury, the role of complement in renal tubular damage has not been evaluated. We investigated the association between complement activation and tubulointerstitial fibrosis. METHODS/STUDY POPULATION: Patients with LN were selected randomly between July 2014 - July 2016. Chromogenic immunohistochemistry was performed on formalin-fixed, paraffin-embedded, 4-µm human renal biopsy secti

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9

Pichler, R. H., N. Franceschini, B. A. Young, et al. "Pathogenesis of cyclosporine nephropathy: roles of angiotensin II and osteopontin." Journal of the American Society of Nephrology 6, no. 4 (1995): 1186–96. http://dx.doi.org/10.1681/asn.v641186.

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Low-salt-diet, cyclosporine (CsA; 15 mg/kg per day)-treated rats develop striped interstitial fibrosis, arteriolar hyalinosis, and azotemia similar to the chronic nephropathy observed in humans. To examine the role of angiotensin II in this model, rats on a low-salt diet were given CsA, CsA and the angiotensin II receptor Type I antagonist Losartan (10 mg/kg per day), CsA and hydralazine/furosemide, or vehicle. At Day 35, CsA-treated rats had tubular injury, arteriolopathy of the afferent arteriole, increased expression of the monocyte-macrophage adhesive protein osteopontin, interstitial macr

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10

Wang, Hao, Yujiao Deng, Limeng He, Yan Deng, and Wei Zhang. "Renal Interstitial Fibrosis Detected on 18F-AlF-NOTA-FAPI-04 PET/CT in a Patient With Multiple Myeloma." Clinical Nuclear Medicine 48, no. 10 (2023): 896–98. http://dx.doi.org/10.1097/rlu.0000000000004804.

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Abstract 18F-AlF-NOTA-FAPI-04 PET/CT was performed on a 58-year-old woman newly diagnosed with multiple myeloma and acute renal insufficiency. 18F-AlF-NOTA-FAPI-04 PET/CT showed increased FAPI uptake in multiple osteolytic lesions and both kidneys. Subsequent renal aspiration biopsy confirmed renal interstitial fibrosis due to subacute tubular interstitial injury. This case suggests that 18F-AlF-NOTA-FAPI-04 PET/CT may be valuable in the evaluation of renal interstitial fibrosis in patients with multiple myeloma.

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11

Shappell, S. B., T. Gurpinar, J. Lechago, W. N. Suki, and L. D. Truong. "Chronic obstructive uropathy in severe combined immunodeficient (SCID) mice: lymphocyte infiltration is not required for progressive tubulointerstitial injury." Journal of the American Society of Nephrology 9, no. 6 (1998): 1008–17. http://dx.doi.org/10.1681/asn.v961008.

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Progressive renal injury in humans and experimental animal models is characterized by tubular atrophy, infiltration of mononuclear inflammatory cells, and interstitial fibrosis. Permanent unilateral ureter ligation represents a reproducible model for investigating mechanisms of progressive kidney injury, and in the rat is characterized by tubular epithelial cell proliferation followed by apoptosis and progressive infiltration of monocytes and lymphocytes. Nevertheless, whether monocytes or lymphocytes play a dominant role in causing tubulointerstitial damage remains to be elucidated. In the cu

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12

Wen, Jin, Zhengwei Ma, Man J. Livingston, et al. "Decreased secretion and profibrotic activity of tubular exosomes in diabetic kidney disease." American Journal of Physiology-Renal Physiology 319, no. 4 (2020): F664—F673. http://dx.doi.org/10.1152/ajprenal.00292.2020.

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Tubular changes contribute to the development of renal pathologies in diabetic kidney disease (DKD), including interstitial fibrosis. It is unclear how tubular cells relay signals to interstitial fibroblasts. Recently, exosomes have been recognized as crucial mediators of intercellular communication. We hypothesized that exosomes secreted from tubular cells may stimulate fibroblasts for interstitial fibrosis in DKD. In this study, we isolated and purified exosomes from the renal cortex of DKD mice and high glucose-treated mouse proximal tubular cells. Compared with nondiabetic mice, exosome se

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13

Eddy, A. A. "Experimental insights into the tubulointerstitial disease accompanying primary glomerular lesions." Journal of the American Society of Nephrology 5, no. 6 (1994): 1273–87. http://dx.doi.org/10.1681/asn.v561273.

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Although chronic progressive tubulointerstitial (TI) disease plays a critical role in the outcome of patients with primary glomerular lesions, the basic mechanisms that generate the TI damage remain unclear. This review focuses on recent insights into this process that originate primarily from studies of animal models of glomerular injury. The acute phase, which is often clinically silent, is characterized by tubular epithelial cell injury and interstitial inflammation. Proposed mediators of tubular injury include antibodies, lysosomal enzymes, obstruction, reactive oxygen metabolites, and com

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14

Forbes, Michael S., Barbara A. Thornhill, Jordan J. Minor, Katherine A. Gordon, Carolina I. Galarreta, and Robert L. Chevalier. "Fight-or-flight: murine unilateral ureteral obstruction causes extensive proximal tubular degeneration, collecting duct dilatation, and minimal fibrosis." American Journal of Physiology-Renal Physiology 303, no. 1 (2012): F120—F129. http://dx.doi.org/10.1152/ajprenal.00110.2012.

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Unilateral ureteral obstruction (UUO) is the most widely used animal model of progressive renal disease. Although renal interstitial fibrosis is commonly used as an end point, recent studies reveal that obstructive injury to the glomerulotubular junction leads to the formation of atubular glomeruli. To quantitate the effects of UUO on the remainder of the nephron, renal tubular and interstitial responses were characterized in mice 7 and 14 days after UUO or sham operation under anesthesia. Fractional proximal tubular mass, cell proliferation, and cell death were measured by morphometry. Supero

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15

Muramatsu, Masaki, Yoji Hyodo, Abigail Lee, et al. "Transplant nephrectomy; pathological features of 124 consecutive cases in a single center study over 10 years." Journal of Nephropathology 8, no. 3 (2019): 23. http://dx.doi.org/10.15171/jnp.2019.23.

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Background: Transplant nephrectomy (TN) is not commonly performed but it may be essential for several indications. Objectives: This study details an in-depth evaluation of the histological changes present in TN specimens. Patients and Methods: We identified 124 consecutive TN cases between 2004 and 2014. The indication for TN was divided into four groups: acute graft loss without significant blood flow (AGL group- 47 cases); suspected ongoing rejection or graft intolerance syndrome (Rej/GIS group44 cases); infection (INF group- 24 cases); and miscellaneous reasons (MIS group- 9 cases). We exam

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16

Wang, S., M. Wu, L. Chiriboga, et al. "OP0043 RENAL TUBULAR COMPLEMENT C9 DEPOSITION IS ASSOCIATED WITH RENAL TUBULAR DAMAGE AND FIBROSIS IN LUPUS NEPHRITIS." Annals of the Rheumatic Diseases 79, Suppl 1 (2020): 28.2–29. http://dx.doi.org/10.1136/annrheumdis-2020-eular.2394.

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Background:Tubulointerstitial damage in lupus nephritis (LN) is a strong predictor of progression to chronic kidney disease and end stage renal disease (ESRD). While prior studies showed complement activation mediates glomerular injury (1), the role of complement in renal tubular damage has not been evaluated.Objectives:To investigate the association between complement activation and tubulointerstitial fibrosis. Specifically, to study the role of tubular complement C9 deposition as a marker of tubular damage and fibrosis in LN.Methods:LN biopsies stored in the pathology department between July

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17

Wei, Qingqing, Jennifer Su, Guie Dong, Ming Zhang, Yuqing Huo, and Zheng Dong. "Glycolysis inhibitors suppress renal interstitial fibrosis via divergent effects on fibroblasts and tubular cells." American Journal of Physiology-Renal Physiology 316, no. 6 (2019): F1162—F1172. http://dx.doi.org/10.1152/ajprenal.00422.2018.

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Renal interstitial fibrosis is a common pathological feature of chronic kidney disease that may involve changes of metabolism in kidney cells. In the present study, we first showed that blockade of glycolysis with either dichloroacetate (DCA) or shikonin to target different glycolytic enzymes reduced renal fibrosis in a mouse model of unilateral ureteral obstruction (UUO). Both inhibitors evidently suppressed the induction of fibronectin and collagen type I in obstructed kidneys, with DCA also showing inhibitory effects on collagen type IV and α-smooth muscle actin (α-SMA). Histological examin

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18

Gupta, Kanishk. "Karyomegalic Interstitial Nephritis-A Rare Cause Of Chronic Tubulointerstitial Nephritis." Nephrology & Renal Therapy 6, no. 3 (2020): 1–3. http://dx.doi.org/10.24966/nrt-7313/100042.

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Karyomegalic Interstitial Nephritis (KIN) is a rare disease, which usually presents with slowly progressive chronic kidney disease, eventually leading to end stage renal disease in early adulthood. Histological findings consist of enlarged and hyperchromatic nuclei in scattered tubular epithelial cells throughout the nephron accompanied by interstitial fibrosis around atrophic tubules.

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Mao, Haiping, Zhilian Li, Yi Zhou, et al. "HSP72 attenuates renal tubular cell apoptosis and interstitial fibrosis in obstructive nephropathy." American Journal of Physiology-Renal Physiology 295, no. 1 (2008): F202—F214. http://dx.doi.org/10.1152/ajprenal.00468.2007.

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Although heat shock protein 72 kDa (HSP72) protects tubular epithelium from a variety of acute insults, its role in chronic renal injury and fibrosis is poorly characterized. In this study, we tested the hypothesis that HSP72 reduces apoptosis and epithelial-to-mesenchymal transition (EMT), important contributors to tubular cell injury in vitro and in vivo. In rats, orally administered geranylgeranylacetone (GGA), an agent that selectively induces HSP72, markedly reduced both apoptosis and cell proliferation in tubular epithelium and decreased both interstitial fibroblast accumulation and coll

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Warner, Gina M., Jingfei Cheng, Bruce E. Knudsen, et al. "Genetic deficiency of Smad3 protects the kidneys from atrophy and interstitial fibrosis in 2K1C hypertension." American Journal of Physiology-Renal Physiology 302, no. 11 (2012): F1455—F1464. http://dx.doi.org/10.1152/ajprenal.00645.2011.

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Although the two-kidney, one-clip (2K1C) model is widely used as a model of human renovascular hypertension, mechanisms leading to the development of fibrosis and atrophy in the cuffed kidney and compensatory hyperplasia in the contralateral kidney have not been defined. Based on the well-established role of the transforming growth factor (TGF)-β signaling pathway in renal fibrosis, we tested the hypothesis that abrogation of TGF-β/Smad3 signaling would prevent fibrosis in the cuffed kidney. Renal artery stenosis (RAS) was established in mice with a targeted disruption of exon 2 of the Smad3 g

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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 (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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Haas, Mark. "Chronic allograft nephropathy or interstitial fibrosis and tubular atrophy." Current Opinion in Nephrology and Hypertension 23, no. 3 (2014): 245–50. http://dx.doi.org/10.1097/01.mnh.0000444811.26884.2d.

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VIELHAUER, VOLKER, HANS-JOACHIM ANDERS, MATTHIAS MACK, et al. "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 (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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Kuruş, Meltem, Murat Ugras, and Mukaddes Esrefoglu. "Effect of resveratrol on tubular damage and interstitial fibrosis in kidneys of rats exposed to cigarette smoke." Toxicology and Industrial Health 25, no. 8 (2009): 539–44. http://dx.doi.org/10.1177/0748233709346755.

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The aim of this study was to evaluate the effect of resveratrol on kidney tissue of rats exposed to cigarette smoke. Forty adult male Wistar Albino rats were divided into four groups. Animals in group 1 was the control group. For 6 weeks, group 2 was exposed to cigarette smoke; group 3 received daily intraperitoneal injections of resveratrol (10 mg/kg/d); and group 4 was exposed to both cigarette smoke and intraperitoneal resveratrol. All rats were sacrificed with cervical dislocation. The kidney tissues were obtained, fixed in Bouin’s fixative and embeded in paraffin blocks. Samples were sect

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Kimura, Kuniko, Masayuki Iwano, Debra F. Higgins та ін. "Stable expression of HIF-1α in tubular epithelial cells promotes interstitial fibrosis". American Journal of Physiology-Renal Physiology 295, № 4 (2008): F1023—F1029. http://dx.doi.org/10.1152/ajprenal.90209.2008.

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Chronic hypoxia accelerates renal fibrosis. The chief mediator of the hypoxic response is hypoxia-inducible factor 1 (HIF-1) and its oxygen-sensitive component HIF-1α. HIF-1 regulates a wide variety of genes, some of which are closely associated with tissue fibrosis. To determine the specific role of HIF-1 in renal fibrosis, we generated a knockout mouse in which tubular epithelial expression of von Hippel-Lindau tumor suppressor (VHL), which acts as a ubiquitin ligase to promote proteolysis of HIF-1α, was targeted. We investigated the effect of VHL deletion (i.e., stable expression of HIF-1α)

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Burdmann, E. A., T. F. Andoh, C. C. Nast, et al. "Prevention of experimental cyclosporin-induced interstitial fibrosis by losartan and enalapril." American Journal of Physiology-Renal Physiology 269, no. 4 (1995): F491—F499. http://dx.doi.org/10.1152/ajprenal.1995.269.4.f491.

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The pathogenesis of renal scarring in chronic cyclosporin nephropathy is unknown. In this study, we evaluated the effects of renin-angiotensin system blockade by enalapril and losartan in a salt-dependent model of cyclosporin-associated chronic tubulointerstitial fibrosis (TIF). Rats kept on normal or low-salt diet were given cyclosporin, cyclosporin+enalapril, cyclosporin+losartan, cyclosporin+enalapril#losartan, or vehicle for 14 and 28 days. Cyclosporin reduced glomerular filtration rate (GFR) in rats fed either diet, but only salt-depleted animals developed significant TIF. Cyclosporin als

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Pang, Maoyin, Jagan Kothapally, Haiping Mao, et al. "Inhibition of histone deacetylase activity attenuates renal fibroblast activation and interstitial fibrosis in obstructive nephropathy." American Journal of Physiology-Renal Physiology 297, no. 4 (2009): F996—F1005. http://dx.doi.org/10.1152/ajprenal.00282.2009.

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Activation of renal interstitial fibroblasts is critically involved in the development of tubulointerstitial fibrosis in chronic kidney diseases. In this study, we investigated the effect of trichostatin A (TSA), a specific histone deacetylase (HDAC) inhibitor, on the activation of renal interstitial fibroblasts in a rat renal interstitial fibroblast line (NRK-49F) and the development of renal fibrosis in a murine model of unilateral ureteral obstruction (UUO) . α-Smooth muscle actin (α-SMA) and fibronectin, two hallmarks of fibroblast activation, were highly expressed in cultured NRK-49F cell

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Quimby, Jessica M., Shannon M. McLeland, Rachel E. Cianciolo, et al. "Frequency of histologic lesions in the kidneys of cats without kidney disease." Journal of Feline Medicine and Surgery 24, no. 12 (2022): e472-e480. http://dx.doi.org/10.1177/1098612x221123768.

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Objectives In humans, renal aging is associated with an increased frequency of glomerulosclerosis, interstitial fibrosis, inflammation and tubular atrophy. The purpose of this study was to describe the frequency of renal histopathologic lesions in cats without kidney disease. Methods A cross-sectional study of archival kidney tissue from 74 cats without kidney disease (serum creatinine <1.6 mg/dl; urine specific gravity >1.035) was carried out: 0–4 years (young, n = 18); 5–9 years (mature, n = 16); 10–14 years (senior, n = 34), 15+ years (geriatric, n = 6). Glomerulosclerosis, tubular at

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Rekhtina, I. G., E. V. Kazarina, E. S. Stolyarevich, et al. "Morphological and immunohistochemical predictors of renal response to therapy patients with myeloma cast nephropathy and dialysis-dependent acute kidney injury." Terapevticheskii arkhiv 92, no. 7 (2020): 63–69. http://dx.doi.org/10.26442/00403660.2020.07.000776.

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Aim.Reveal morphological and immunohistochemical predictors of reversibility of dialysis-dependent acute kidney injury (AKI) in patients with myeloma cast nephropathy (MCN) based on the study of kidney biopsy. Materials and methods.Renal pathological findings were studied in 36 patients with MCN and dialysis-dependent stage 3 AKI (AKIN, 2012). The study of biopsy samples was performed by a semi-quantitative and quantitative analysis using computer morphometry. The expression of E-cadherin, vimentin and-smooth muscle actin was determined immunohistochemically in the tubular cells and inte

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Sun, Ke, Zhenliang Fan, and Junfeng Fan. "A study on the mechanism of cordycepin in regulating autophagy and alleviating renal tubular interstitial fibrosis." Tropical Journal of Pharmaceutical Research 23, no. 3 (2024): 529–35. http://dx.doi.org/10.4314/tjpr.v23i3.6.

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Purpose: To elucidate the role of cordycepin in modulating autophagy and mitigating renal tubular interstitial fibrosis in a rat model of unilateral ureteral obstruction (UUO). Methods: Forty male Sprague-Dawley (SD) rats were assigned to four groups: control, sham, UUO and cordyceps-treated groups (10 rats per group). The UUO and cordyceps groups underwent surgery to induce unilateral ureteral obstruction. The cordyceps group received intravenous cordycepin (10 mg/kg) daily for 14 days, while the control and UUO groups received normal saline. Histopathological examination, assessment of fibro

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Debelle, Frédéric D., Joëlle L. Nortier, Eric G. De Prez, et al. "Aristolochic Acids Induce Chronic Renal Failure with Interstitial Fibrosis in Salt-Depleted Rats." Journal of the American Society of Nephrology 13, no. 2 (2002): 431–36. http://dx.doi.org/10.1681/asn.v132431.

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ABSTRACT. Chinese-herb nephropathy (CHN) is a rapidly progressive renal fibrosis associated with the intake of a Chinese herb (Aristolochia fangchi) containing nephrotoxic and carcinogenic aristolochic acids (AA). This study attempted to reproduce the main features of human CHN (renal failure, tubular atrophy, and interstitial fibrosis) in a rat model similar to that of cyclosporin-induced nephropathy. Salt-depleted male Wistar rats received daily subcutaneous injections of either 1 mg/kg body wt AA (low-dose AA group), 10 mg/kg body wt AA (high-dose AA group), or vehicle (control group) for 3

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Tampe, Désirée, Laura Schridde, Peter Korsten, et al. "Different Patterns of Kidney Fibrosis Are Indicative of Injury to Distinct Renal Compartments." Cells 10, no. 8 (2021): 2014. http://dx.doi.org/10.3390/cells10082014.

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Kidney fibrosis is a common manifestation and hallmark of a wide variety of chronic kidney disease (CKD) that appears in different morphological patterns, suggesting distinct pathogenic causes. Broad macroscopically visible scars are the sequelae of severe focal injury and complete parenchymal destruction, reflecting a wound healing response as a consequence of infarction. In the kidney, chronic glomerular injury leads to atrophy of the corresponding tubule, degeneration of this specific nephron, and finally interstitial fibrosis/tubular atrophy (IF/TA). Compared to this glomerulus-induced foc

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Ranganathan, Punithavathi, Calpurnia Jayakumar, and Ganesan Ramesh. "Proximal tubule-specific overexpression of netrin-1 suppresses acute kidney injury-induced interstitial fibrosis and glomerulosclerosis through suppression of IL-6/STAT3 signaling." American Journal of Physiology-Renal Physiology 304, no. 8 (2013): F1054—F1065. http://dx.doi.org/10.1152/ajprenal.00650.2012.

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Acute kidney injury-induced organ fibrosis is recognized as a major risk factor for the development of chronic kidney disease, which remains one of the leading causes of death in the developed world. However, knowledge on molecules that may suppress the fibrogenic response after injury is lacking. In ischemic models of acute kidney injury, we demonstrate a new function of netrin-1 in regulating interstitial fibrosis. Acute injury was promptly followed by a rise in serum creatinine in both wild-type and netrin-1 transgenic animals. However, the wild-type showed a slow recovery of kidney functio

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Huang, Ming, Shuai Zhu, Huihui Huang, et al. "Integrin-Linked Kinase Deficiency in Collecting Duct Principal Cell Promotes Necroptosis of Principal Cell and Contributes to Kidney Inflammation and Fibrosis." Journal of the American Society of Nephrology 30, no. 11 (2019): 2073–90. http://dx.doi.org/10.1681/asn.2018111162.

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BackgroundNecroptosis is a newly discovered cell death pathway that plays a critical role in AKI. The involvement of integrin-linked kinase (ILK) in necroptosis has not been studied.MethodsWe performed experiments in mice with an Ilk deletion in collecting duct (CD) principal cells (PCs), and cultured tubular epithelial cells treated with an ILK inhibitor or ILK siRNA knockdown.ResultsIlk deletion in CD PCs resulted in acute tubular injury and early mortality in mice. Progressive interstitial fibrosis and inflammation associated with the activation of the canonical TGF-β signaling cascade were

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Wang, Xiaohua, Yang Zhou, Ruoyun Tan, et al. "Mice lacking the matrix metalloproteinase-9 gene reduce renal interstitial fibrosis in obstructive nephropathy." American Journal of Physiology-Renal Physiology 299, no. 5 (2010): F973—F982. http://dx.doi.org/10.1152/ajprenal.00216.2010.

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Matrix metalloproteinase-9 (MMP-9) is one of the major components of the matrix proteolytic network, and its role in the pathogenesis of renal interstitial fibrosis remains largely unknown. Here, we demonstrate that ablation of MMP-9 attenuated renal interstitial fibrotic lesions in obstructive nephropathy. Mice lacking MMP-9 were less likely to develop morphological injury, which was characterized by a reduced disruption of tubular basement membrane (TBM) and expression of fibronectin as well as deposition of total tissue collagen in the kidneys after sustained ureteral obstruction compared w

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Gui, Yuan, and Chunsun Dai. "mTOR Signaling in Kidney Diseases." Kidney360 1, no. 11 (2020): 1319–27. http://dx.doi.org/10.34067/kid.0003782020.

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The mammalian target of rapamycin (mTOR), a serine/threonine protein kinase, is crucial in regulating cell growth, metabolism, proliferation, and survival. Under physiologic conditions, mTOR signaling maintains podocyte and tubular cell homeostasis. In AKI, activation of mTOR signaling in tubular cells and interstitial fibroblasts promotes renal regeneration and repair. However, constitutive activation of mTOR signaling in kidneys results in the initiation and progression of glomerular hypertrophy, interstitial fibrosis, polycystic kidney disease, and renal cell carcinoma. Here, we summarize t

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Yamashita, Noriyuki, Tetsuro Kusaba, Tomohiro Nakata, et al. "Intratubular epithelial-mesenchymal transition and tubular atrophy after kidney injury in mice." American Journal of Physiology-Renal Physiology 319, no. 4 (2020): F579—F591. http://dx.doi.org/10.1152/ajprenal.00108.2020.

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Tubular atrophy is a common pathological feature of kidney fibrosis. Although fibroblasts play a predominant role in tissue fibrosis, the role of repairing tubular epithelia in tubular atrophy is unclear. We demonstrated the essential role of focal adhesion kinase (FAK)-mediated intratubular epithelial-mesenchymal transition (EMT) in the pathogenesis of tubular atrophy after severe ischemia-reperfusion injury (IRI). Actively proliferating tubular epithelia undergoing intratubular EMT were noted in the acute phase of severe IRI, resulting in tubular atrophy in the chronic phase, reflecting fail

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Kida, Yujiro, Kinji Asahina, Hirobumi Teraoka, Inna Gitelman, and Tetsuji Sato. "Twist Relates to Tubular Epithelial-Mesenchymal Transition and Interstitial Fibrogenesis in the Obstructed Kidney." Journal of Histochemistry & Cytochemistry 55, no. 7 (2007): 661–73. http://dx.doi.org/10.1369/jhc.6a7157.2007.

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Epithelial-mesenchymal transition (EMT) is a critical step in renal fibrosis. It has been recently reported that a transcription factor, Twist, plays a pivotal role in metastasis of breast tumors by inducing EMT. In this study, we examined whether Twist relates to renal fibrogenesis including EMT of tubular epithelia, evaluating Twist expression level in the unilateral ureteral obstruction (UUO) model. Kidneys of mice subjected to UUO were harvested 1, 3, 7, and 10 days after obstruction. Compared with control kidneys, Twist mRNA-level significantly increased 3 days after UUO (UUO day 3 kidney

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Morales, Enrique, Hernando Trujillo, Teresa Bada, et al. "What is the value of repeat kidney biopsies in patients with lupus nephritis?" Lupus 30, no. 1 (2020): 25–34. http://dx.doi.org/10.1177/0961203320965703.

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Introduction Recent studies with protocol biopsies have shown a mismatch between clinical and histological remission in lupus nephritis (LN). We aimed to evaluate histological changes in repeat kidney biopsies by clinical indication in patients with LN. Methods We analyzed 107 patients with LN in which a kidney biopsy was performed between 2008 and 2018. Of those, we included 26 (24.2%) who had ≥2 kidney biopsies. Classification was done according to the International Society of Nephrology/Renal Pathology Society. Results Mean time between biopsies was 71.5 ± 10.7 months. 73.1% of patients pre

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Ginley, Brandon, Kuang-Yu Jen, Seung Seok Han, et al. "Automated Computational Detection of Interstitial Fibrosis, Tubular Atrophy, and Glomerulosclerosis." Journal of the American Society of Nephrology 32, no. 4 (2021): 837–50. http://dx.doi.org/10.1681/asn.2020050652.

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BackgroundInterstitial fibrosis, tubular atrophy (IFTA), and glomerulosclerosis are indicators of irrecoverable kidney injury. Modern machine learning (ML) tools have enabled robust, automated identification of image structures that can be comparable with analysis by human experts. ML algorithms were developed and tested for the ability to replicate the detection and quantification of IFTA and glomerulosclerosis that renal pathologists perform.MethodsA renal pathologist annotated renal biopsy specimens from 116 whole-slide images (WSIs) for IFTA and glomerulosclerosis. A total of 79 WSIs were

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Hart, Allyson, Scott Jackson, Bertram L. Kasiske, et al. "Uric Acid and Allograft Loss From Interstitial Fibrosis/Tubular Atrophy." Transplantation 97, no. 10 (2014): 1066–71. http://dx.doi.org/10.1097/01.tp.0000440952.29757.66.

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Cui, Wenpeng, Hasiyeti Maimaitiyiming, Xinyu Qi, et al. "Increasing cGMP-dependent protein kinase activity attenuates unilateral ureteral obstruction-induced renal fibrosis." American Journal of Physiology-Renal Physiology 306, no. 9 (2014): F996—F1007. http://dx.doi.org/10.1152/ajprenal.00657.2013.

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Our previous studies support the protective effect of cGMP and cGMP-dependent protein kinase I (PKG-I) pathway on the development of renal fibrosis. Therefore, in the present studies, we determined whether pharmacologically or genetically increased PKG activity attenuates renal fibrosis in a unilateral ureteral obstruction (UUO) model and also examined the mechanisms involved. To increase PKG activity, we used the phosphodiesterase 5 inhibitor sildenafil and PKG transgenic mice. UUO model was induced in wild-type or PKG-I transgenic mice by ligating the left lateral ureteral and the renal fibr

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Cahyawati, Putu Nita, Ngatidjan ., Dwi Cahyani Ratna Sari, et al. "SIMVASTATIN ATTENUATES RENAL FAILURE IN MICE WITH A 5/6 SUBTOTAL NEPHRECTOMY." International Journal of Pharmacy and Pharmaceutical Sciences 9, no. 5 (2017): 12. http://dx.doi.org/10.22159/ijpps.2017v9i5.12261.

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Objective: The objective of this study to investigate the effect of simvastatin on kidney fibrosis in mice with a 5/6 subtotal nephrectomy.Methods: Thirty adults (3 mo old) male Swiss mice were submitted to a 5/6 subtotal nephrectomy and studied after 14 d. Animals were divided into five groups: 5/6 subtotal nephrectomy (SN, n=6), sham operation (SH, n=6), simvastatin 5.2 mg/kg body weight (SIM-1, n=6), simvastatin 10.4 mg/kg body weight (SIM-2, n=6), and simvastatin 20.8 mg/kg body weight (SIM-3, n=6) groups. At sacrifice, kidneys were harvested for morphology (glomerulosclerosis (GS), tubula

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Wilson, Parker C., Michael Kashgarian, and Gilbert Moeckel. "Interstitial inflammation and interstitial fibrosis and tubular atrophy predict renal survival in lupus nephritis." Clinical Kidney Journal 11, no. 2 (2017): 207–18. http://dx.doi.org/10.1093/ckj/sfx093.

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Yao, Lan, M. Frances Wright, Brandon C. Farmer, et al. "Fibroblast-specific plasminogen activator inhibitor-1 depletion ameliorates renal interstitial fibrosis after unilateral ureteral obstruction." Nephrology Dialysis Transplantation 34, no. 12 (2019): 2042–50. http://dx.doi.org/10.1093/ndt/gfz050.

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Abstract Background Plasminogen activator inhibitor-1 (PAI-1) expression increases extracellular matrix deposition and contributes to interstitial fibrosis in the kidney after injury. While PAI-1 is ubiquitously expressed in the kidney, we hypothesized that interstitial fibrosis is strongly dependent on fibroblast-specific PAI-1 (fbPAI-1). Methods Tenascin C Cre (TNC Cre) and fbPAI-1 knockdown (KD) mice with green fluorescent protein (GFP) expressed within the TNC construct underwent unilateral ureteral obstruction and were sacrificed 10 days later. Results GFP+ cells in fbPAI-1 KD mice showed

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Fine, L. G., and J. T. Norman. "Renal growth responses to acute and chronic injury: routes to therapeutic intervention." Journal of the American Society of Nephrology 2, no. 10 (1992): S206. http://dx.doi.org/10.1681/asn.v210s206.

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Knowledge of the control of cell growth and extracellular matrix deposition has assumed center stage in the understanding of how the diseased kidney responds to injury. After acute tubular injury, there may be reversible, partial depolarization of renal cells or cell necrosis. The latter requires a regenerative response, which could be under the control of growth factors such as epidermal growth factor (EGF). Up-regulation of EGF receptors on viable cells provides the cell with an enhanced growth response despite a reduction in EGF production by the kidney. Acute glomerular injury involves a h

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Yang, Junwei, and Youhua Liu. "Delayed administration of hepatocyte growth factor reduces renal fibrosis in obstructive nephropathy." American Journal of Physiology-Renal Physiology 284, no. 2 (2003): F349—F357. http://dx.doi.org/10.1152/ajprenal.00154.2002.

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Hepatocyte growth factor (HGF) is a renotropic protein that elicits antifibrogenic activity by preventing the activation of matrix-producing myofibroblast cells in animal models of chronic renal diseases. However, whether a delayed administration of HGF can still attenuate renal fibrosis remains uncertain. In this study, we examined the therapeutic potential of exogenous HGF on an established renal interstitial fibrosis induced by unilateral ureteral obstruction (UUO). Three days after UUO, the obstructed kidneys displayed interstitial fibrotic lesions with characteristic features of an establ

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Torsello, Barbara, Sofia De Marco, Silvia Bombelli, et al. "High glucose induces an activated state of partial epithelial-mesenchymal transition in human primary tubular cell cultures." PLOS ONE 18, no. 2 (2023): e0279655. http://dx.doi.org/10.1371/journal.pone.0279655.

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Tubulointerstitial fibrosis is observed in diabetic nephropathy. It is still debated whether tubular cells, undergoing epithelial-mesenchymal transition (EMT) in high glucose (HG) conditions, may contribute to interstitial fibrosis development. In this study, we investigated the phenotypic and molecular EMT-like changes and the alteration of inflammatory and fibrogenic secretome induced by HG in human primary tubular cell cultures. Taking advantage of this in vitro cell model composed of proximal and distal tubular cells, we showed that HG-treated tubular cells acquired a fibroblast-like morph

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Ma, Frank Y., Jian Liu, A. Richard Kitching, Carl L. Manthey, and David J. Nikolic-Paterson. "Targeting renal macrophage accumulation via c-fms kinase reduces tubular apoptosis but fails to modify progressive fibrosis in the obstructed rat kidney." American Journal of Physiology-Renal Physiology 296, no. 1 (2009): F177—F185. http://dx.doi.org/10.1152/ajprenal.90498.2008.

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The role of macrophages in promoting interstitial fibrosis in the obstructed kidney is controversial. Macrophage depletion studies in the unilateral ureter obstruction (UUO) model have produced opposing results, presumably reflecting the subtleties of the individual depletion methods used. To address this question, we targeted the macrophage colony-stimulating factor receptor, c- fms, which is uniquely expressed by cells of the monocyte/macrophage lineage. Administration of 5, 12.5, or 30 mg/kg (bid) of a selective inhibitor of c- fms kinase activity (fms-I) resulted in a dose-dependent inhibi

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Jung, Hyun Jin, Hyun-Jin An, Mi-Gyeong Gwon, et al. "Anti-Fibrotic Effect of Synthetic Noncoding Oligodeoxynucleotide for Inhibiting mTOR and STAT3 via the Regulation of Autophagy in an Animal Model of Renal Injury." Molecules 27, no. 3 (2022): 766. http://dx.doi.org/10.3390/molecules27030766.

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Renal fibrosis is a common process of various kidney diseases. Autophagy is an important cell biology process to maintain cellular homeostasis. In addition, autophagy is involved in the pathogenesis of various renal disease, including acute kidney injury, glomerular diseases, and renal fibrosis. However, the functional role of autophagy in renal fibrosis remains poorly unclear. The mammalian target of rapamycin (mTOR) plays a negative regulatory role in autophagy. Signal transducer and activator of transcription 3 (STAT3) is an important intracellular signaling that may regulate a variety of i

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