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Articles de revues sur le sujet « Fibrosi renale »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 31 juillet 2025

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1

Curci, C., and G. Castellano. "Fibrosi renale ed anemia: una storia tutta da scoprire." Giornale di Clinica Nefrologica e Dialisi 24, no. 1 (2018): 27–28. http://dx.doi.org/10.33393/gcnd.2012.1111.

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Ad oggi l'origine dei fibroblasti, le principali cellule responsabili dello sviluppo della fibrosi renale, è ancora incerta. In un recente lavoro pubblicato da Asada e colleghi, gli Autori dimostrano che la maggior parte dei fibroblasti secernenti eritropoietina nel rene normale hanno un'origine extra renale e provengono da cellule della Cresta Neurale. Durante lo sviluppo della fibrosi renale, queste cellule trans-differenziano in miofibroblasti, perdendo la loro capacità intrinseca di produrre eritropoietina. Questi interessanti dati potrebbero rappresentare il punto di partenza per lo svilu

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Lombardi, Duccio. "Rigenerazione e Proteinuria, Quando L'albumina Fa La Differenza." Giornale di Clinica Nefrologica e Dialisi 26, no. 1 (2014): 65–68. http://dx.doi.org/10.33393/gcnd.2014.864.

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Nella malattia renale cronica, il rischio di fallimento d’organo dipende dal grado di severità della proteinuria, la quale è determinata dal numero di podociti persi e dalla conseguente fibrosi glomerulare. Esistono, tuttavia, numerose evidenze cliniche e sperimentali che suggeriscono la possibilità di remissione della malattia renale e, in alcuni casi, persino di regressione del danno, quando ancora l’istologia dell’organo non risulti totalmente compromessa. Tali risultati sono ottenuti in particolare mediante l’impiego di terapie con effetti anti-proteinurici. Nuove evidenze sperimentali sug

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3

Di Lullo, L., F. Floccari, R. Rivera, et al. "La patologia del pericardio e la malattia renale cronica." Giornale di Clinica Nefrologica e Dialisi 24, no. 2 (2018): 62–70. http://dx.doi.org/10.33393/gcnd.2012.1141.

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I pazienti affetti da malattia renale cronica possono andare incontro a tutta una serie di patologie che colpiscono il pericardio ma, sicuramente, alcune entità nosologiche sono più frequenti di altre. Gli ultimi decenni hanno assistito, per fortuna nostra e dei nostri pazienti, a un netto miglioramento per quanto concerne i protocolli terapeutici per i pazienti nefropatici e le forme tipiche di pericardite uremica, così frequenti negli anni passati, sono ormai uno sbiadito ricordo. È tuttora frequente osservare pazienti con versamento pericardico (idiopatico, ovvero secondario a malattie sist

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Masola, V., S. Granata, M. Proglio, G. Gambaro, A. Lupo, and G. Zaza. "Eparanasi: un nuovo biomarker di fibrosi e un potenziale target farmacologico per ridurre la progressione del danno renale cronico." Giornale di Clinica Nefrologica e Dialisi 24, no. 2 (2018): 10–15. http://dx.doi.org/10.33393/gcnd.2012.1131.

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Il trattamento poli-farmacologico ha determinato, nel corso degli anni, un significativo rallentamento della progressione della malattia renale cronica verso lo stadio di uremia terminale, ma siamo ancora distanti dallo sviluppo di interventi terapeutici in grado di bloccare questo inesorabile e irreversibile processo. Studi clinico-patologici hanno chiaramente dimostrato che il principale elemento coinvolto nel danno renale è la fibrosi tubulo-interstiziale e che il meccanismo patogenetico alla base di questa condizione ha inizio in larga parte nel compartimento tubulare. In particolare, il p

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Wolf, G., and G. Lehmann. "Knochenhistologie bei renaler Osteodystrophie." Osteologie 17, no. 03 (2008): 107–11. http://dx.doi.org/10.1055/s-0037-1619855.

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ZusammenfassungChronische Nierenfunktionseinschränkungen führen am Knochen zu Stoffwechsel- und Strukturschäden, deren differenzierte Beurteilung vor allem durch die histologische Aufarbeitung von Knochenbioptaten möglich ist. Die internationale Klassifikation unterscheidet vier Formen der renalen Osteodystrophie (ROD). Dabei wird zwischen renalem Hyperparathyreoidismus (Osteitis fibrosa), Osteomalazie, gemischter urämischer Osteodystrophie und adynamer renaler Knochenerkrankung unterschieden. In der Arbeit werden die Methoden der Knochenentnahme und -bearbeitung, typische histologische Befund

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D'Attoma, N., E. Residori, R. Mariotto, R. Cerini, M. Gregianin, and A. Lotto. "L'imaging della fibrosi retroperitoneale primitiva: Primitive retroperitoneal fibrosis imaging." Urologia Journal 65, no. 2 (1998): 276–86. http://dx.doi.org/10.1177/039156039806500216.

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Idiopathic retroperitoneal fibrosis (RPF) is characterised by the development of a fibrotic mass in the prelumbar or presacral area which becomes clinically significant when it causes ureteral obstruction. New imaging techniques have improved accuracy of the morphological approach to the disease, but urography and sequential renal scintigraphy are still important for assessing ureteral involvement. The role of imaging techniques is discussed and current diagnostic and therapeutic tools are evaluated.

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Galiza, Aline Xavier Fialho, Luísa Mariano Cerqueira da Silva, Luísa Grecco Correa, et al. "Perfil epidemiológico e alterações anatomopatológicas de biópsias de rins esquerdos de sete cães acometidos por Dioctophyme renale em rim direito." Research, Society and Development 10, no. 6 (2021): e50310615703. http://dx.doi.org/10.33448/rsd-v10i6.15703.

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A dioctofimatose é uma doença causada pelo nematódeo Dioctophyme renale, que acomete principalmente rins direitos de cães e ao penetrar na cápsula renal causa destruição e atrofia do parênquima, podendo restar apenas uma cápsula fibrosa do rim afetado. Dessa forma, buscando estabelecer as condições histológicas do rim contralateral (RCL) dos animais acometidos pela parasitose, o objetivo desse estudo foi descrever o perfil epidemiológico e alterações anatomopatológicas encontradas em biópsias de rins esquerdos de sete cães submetidos a nefrectomia em decorrência de parasitismo por Dioctophyme

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Oelzner, Peter, Kerstin Amann, and Gunter Wolf. "Nierenbeteiligung bei Kollagenosen – Teil 2: Antiphospholipid-Syndrom, primäres Sjögren-Syndrom, systemische Sklerose." Aktuelle Rheumatologie 45, no. 02 (2020): 163–72. http://dx.doi.org/10.1055/a-1089-7347.

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ZusammenfassungRenale Manifestationen bei Antiphospholipid-Syndrom (APS), primärem Sjögren-Syndrom (pSS) und systemischer Sklerose (SSc) unterscheiden sich erheblich in Pathogenese, Histologie, klinischem Erscheinungsbild, Prognose und therapeutischer Konsequenz. Die Häufigkeit APS-assoziierter Nierenveränderungen wird mit 10–40% angegeben. Das APS kann sich an der Niere in Form von renaler Hypertonie, Thrombosen oder Stenosen der Nierenarterien, Niereninfarkten, Nierenvenenthrombose und intrarenaler Vaskulopathie (APS-Nephropathie) manifestieren. Gerade beim sekundären APS ist die Differenzia

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Rossi, Y. A., D. C. Sousa, J. R. Rocha, V. Rodrigues, and F. G. G. Dias. "Fibrous osteodystrophy due to secondary renal hyperparathyroidism in a senile dog." Arquivo Brasileiro de Medicina Veterinária e Zootecnia 74, no. 6 (2022): 1089–95. http://dx.doi.org/10.1590/1678-4162-12713.

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ABSTRACT Renal hyperparathyroidism stands out among the complications of kidney disease in dogs due to phosphorus retention with a predisposition to hypocalcemia, parathyroid hormone stimulation with mobilization of calcium from the bones, characterizing fibrous osteodystrophy, unusual in the elderly. The objective was to report it in 12-year-old Labrador with polyuria, polydipsia, and emesis for five months due to maxillary and mandibular volume increase, followed by loosely fixed teeth, and facial deformity. Blood tests showed anemia, thrombocytosis, azotemia, hypoalbuminemia and hyperphosph

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10

Kommers, Glaucia Denise, Márcia Regina da Silva Ilha, and Claudio Severo Lombardo de Barros. "Dioctofimose em cães: 16 casos." Ciência Rural 29, no. 3 (1999): 517–22. http://dx.doi.org/10.1590/s0103-84781999000300023.

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No período de 1978 a 1996, de um total de 3.259 cães necropsiados, 16 (0,49%) apresentaram parasitismo por Dioctophyma renale. Desses, 12 (75%) eram cães de rua. Em 13 cães (81, 2%), um ou vários parasitas localizavam-se no rim direito. Em 3 casos (18,7%), o parasita foi observado na cavidade abdominal. Nos casos de parasitismo renal, observou-se acentuada atrofia do parênquima, transformando o rim numa bolsa fibrosa contendo o parasita em meio a exsudato necro-hemorrágico semilíquido. Foi observada hipertrofia renal compensatória contralateral em 5 casos. O ciclo evolutivo de D. renale é comp

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11

Shin, Sug Kyun, Do Hun Kim, Heung Su Kim, et al. "Renal Osteodystrophy in Pre-Dialysis Patients: Ethnic Difference?" Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 19, no. 2_suppl (1999): 402–7. http://dx.doi.org/10.1177/089686089901902s65.

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The purpose of the present study is to investigate whether an ethnic difference exists in the incidence of renal osteodystrophy between Asian and Western countries in end-stage renal disease (ESRD) patients. We evaluated bone histology in 58 pre-dialysis patients (28 male, 30 female; mean age: 47.7 years). All patients had bone biopsies with quantitative histomorphometry and sero-logical parameters such as intact PTH, osteocalcin, total alkaline phosphatase, and basal and deferoxamine-stimulated serum aluminum levels. We observed that 91.4% of all evaluated patients showed renal osteodystrophy

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Gu, Yue-Yu, Xu-Sheng Liu, Xiao-Ru Huang, Xue-Qing Yu та Hui-Yao Lan. "TGF-β in renal fibrosis: triumphs and challenges". Future Medicinal Chemistry 12, № 9 (2020): 853–66. http://dx.doi.org/10.4155/fmc-2020-0005.

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Renal fibrosis is a hallmark of chronic kidney disease. Although considerable achievements in the pathogenesis of renal fibrosis have been made, the underlying mechanisms of renal fibrosis remain largely to be explored. Now we have reached the consensus that TGF-β is a master regulator of renal fibrosis. Indeed, TGF-β regulates renal fibrosis via both canonical and noncanonical TGF-β signaling. Moreover, ongoing renal inflammation promotes fibrosis as inflammatory cells such as macrophages, conventional T cells and mucosal-associated invariant T cells may directly or indirectly contribute to r

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Foda, Marwa SaidAbd Elsaed, HassanAbd Elhady Ahmed, YasseinSalahYassein Mohamed, and AhmedRagheb Tawfek. "Renal fibrosis." Menoufia Medical Journal 28, no. 2 (2015): 540. http://dx.doi.org/10.4103/1110-2098.163915.

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14

Zeisberg, Michael, Yohei Maeshima, Barbara Mosterman, and Raghu Kalluri. "Renal Fibrosis." American Journal of Pathology 160, no. 6 (2002): 2001–8. http://dx.doi.org/10.1016/s0002-9440(10)61150-9.

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Zeisberg, Michael, Gary Bonner, Yohei Maeshima, et al. "Renal Fibrosis." American Journal of Pathology 159, no. 4 (2001): 1313–21. http://dx.doi.org/10.1016/s0002-9440(10)62518-7.

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Cho, Min Hyun. "Renal fibrosis." Korean Journal of Pediatrics 53, no. 7 (2010): 735. http://dx.doi.org/10.3345/kjp.2010.53.7.735.

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Schnaper, H. William. "Renal fibrosis." Frontiers in Bioscience 8, no. 5 (2003): e68-86. http://dx.doi.org/10.2741/925.

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Reich, B., F. Hermann, Y. Talke, et al. "Renal fibrosis." Nephrology Dialysis Transplantation 27, suppl 2 (2012): ii44—ii45. http://dx.doi.org/10.1093/ndt/gfs198.

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Valle, Bruna dos Santos, Pamela Caye, Carolina da Fonseca Sapin, et al. "Alterações anatomopatológicas e parâmetros bioquímicos séricos e urinários em cães com diagnóstico de Dioctophyme renale." Research, Society and Development 11, no. 12 (2022): e515111234874. http://dx.doi.org/10.33448/rsd-v11i12.34874.

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Animais acometidos por Dioctophyme renale geralmente são assintomáticos e o diagnóstico definitivo é o exame de imagem e o anatomopatológico. Desta forma, este estudo tem como objetivo descrever os parâmetros bioquímicos de sangue e urina e exames anatomopatológicos de 15 cães diagnosticados com D. renale na região de Pelotas-Rio Grande do Sul-RS. Foram obtidos dados de anamnese e exames laboratoriais sorológicos e urinários de protocolos de atendimento de animais no Hospital de Clínicas Veterinárias da Universidade Federal de Pelotas-UFPel, e análises anatomopatológicas pelo Serviço de oncolo

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Eddy, Allison A. "Scraping fibrosis: UMODulating renal fibrosis." Nature Medicine 17, no. 5 (2011): 553–55. http://dx.doi.org/10.1038/nm0511-553.

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Jenkins, Joseph, Sergey V. Brodsky, Anjali A. Satoskar, Gyongyi Nadasdy, and Tibor Nadasdy. "The Relevance of Periglomerular Fibrosis in the Evaluation of Routine Needle Core Renal Biopsies." Archives of Pathology & Laboratory Medicine 135, no. 1 (2011): 117–22. http://dx.doi.org/10.5858/2009-0484-oar1.1.

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Abstract Context—Renal interstitial fibrosis and, to a lesser extent, sclerotic glomeruli correlate with poor renal function. However, not all nonfunctional glomeruli are sclerotic. Many or most glomeruli with periglomerular fibrosis, while retaining blood flow, probably do not filter; therefore, they may not contribute to renal function. Objective—To examine the relationship of periglomerular fibrosis and the sum of globally sclerotic glomeruli and glomeruli with periglomerular fibrosis (GSG+PF) with interstitial fibrosis and renal function. Design—Native kidney biopsies from 177 patients wit

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Ma, Liang, and Xiaoyong Yu. "Progress of Chinese Medicine in Regulating Altered Lipid Metabolism in Renal Fibrosis." Journal of Contemporary Medical Practice 7, no. 3 (2025): 43–47. https://doi.org/10.53469/jcmp.2025.07(03).08.

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Renal fibrosis leads to progressive impairment of renal structure and function, which is a common pathologic impairment. There are few interventions targeting the mechanisms of fibrosis that can delay renal decompensation in patients. This review highlights the potential “antibiotic” of lipid metabolism and lipoproteins in ameliorating renal fibrosis, some representative targets and several other metabolic modulators with anti-fibrotic effects in the kidney, as well as the roles of fatty acid oxidation, lipids, and lipoprotein synthesis and catabolism in the prophylactic treatment of fibrosis.

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Sun, Yu-Chao, Zhen-Zhen Qiu, Fu-Li Wen, Jin-Quan Yin, and Hao Zhou. "Revealing Potential Diagnostic Gene Biomarkers Associated with Immune Infiltration in Patients with Renal Fibrosis Based on Machine Learning Analysis." Journal of Immunology Research 2022 (April 20, 2022): 1–20. http://dx.doi.org/10.1155/2022/3027200.

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Chronic kidney disease is characterized by the development of renal fibrosis. The basic mechanisms of renal fibrosis have not yet been fully investigated despite significant progress in understanding the etiology of the disease. In this work, the researchers sought to identify potential diagnostic indicators for renal fibrosis. From the GEO database, we were able to acquire two gene expression profiles with publically available data (GSE22459 and GSE76882, respectively) from human renal fibrosis and control samples. 215 renal fibrosis specimens and 124 normal specimens were examined for differ

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Li, Chen, Yuan-Fei Liu, Chong Huang, Yan-Xia Chen, Cheng-Yun Xu, and Yan Chen. "Long noncoding RNA NEAT1 sponges miR-129 to modulate renal fibrosis by regulation of collagen type I." American Journal of Physiology-Renal Physiology 319, no. 1 (2020): F93—F105. http://dx.doi.org/10.1152/ajprenal.00552.2019.

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The long noncoding RNA nuclear enriched abundant transcript 1 (NEAT1) has been reported to promote liver fibrosis progression. However, its molecular mechanism in renal fibrosis was not elucidated. In the present study, an in vitro model of renal fibrosis was established with HK-2 and HKC-8 cells treated with transforming growth factor-β1. C57BL/6 mice were used for the in vivo model with unilateral ureteral obstruction. Our results indicated that NEAT1 and collagen type I levels were significantly upregulated, whereas miR-129 was obviously downregulated, in the progression of renal fibrosis.

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He, Shiyang, Lan Yao, and Jun Li. "Role of MCP-1/CCR2 axis in renal fibrosis: Mechanisms and therapeutic targeting." Medicine 102, no. 42 (2023): e35613. http://dx.doi.org/10.1097/md.0000000000035613.

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Renal fibrosis is a common pathological manifestation in various chronic kidney diseases. Inflammation plays a central role in renal fibrosis development. Owing to their significant participation in inflammation and autoimmunity, chemokines have always been the hot spot and focus of scientific research and clinical intervention. Among the chemokines, monocyte chemoattractant protein-1 (MCP-1), also known as C-C motif chemokine ligand 2, together with its main receptor C–C chemokine receptor type 2 (CCR2) are important chemokines in renal fibrosis. The MCP-1/CCR2 axis is activated when MCP-1 bi

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Chen, Sheng. "circ_000166/miR-296 Aggravates the Process of Diabetic Renal Fibrosis by Regulating the SGLT2 Signaling Pathway in Renal Tubular Epithelial Cells." Disease Markers 2022 (May 16, 2022): 1–10. http://dx.doi.org/10.1155/2022/6103086.

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Diabetic renal fibrosis is a common cause of end-stage renal disease, and the circRNA-miRNA-mRNA network may play an important role in the progression of diabetic nephropathy- (DN-) induced renal fibrosis. In this study, the role of circ_000166/miR-296/SGLT2 in the process of DN-related renal fibrosis was studied by constructing an animal model of DN renal fibrosis via lentiviral transfection, plasmid transfection, and dual-luciferase reporting techniques. Compared with that of normal controls, the expression of circ_000166 in the kidney tissues of DN renal fibrosis mice substantially increase

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Aguirre López, Jesús Roberto, Francisco Trinidad Alberto, Jorge Enrique Sámano Pozos, Nancy Patricia López Llanes, and Francisco Jaime Torres Franco. "Obstrucción Ureteropielica Extrínseca Secundaria a Banda Fibrosa, Una Presentación Rara Descrita en la Literatura." Ciencia Latina Revista Científica Multidisciplinar 8, no. 3 (2024): 7880–90. http://dx.doi.org/10.37811/cl_rcm.v8i3.11984.

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La obstrucción ureteropiélica (UPO) puede tener diversas causas, siendo las bandas fibrosas una causa poco común. Esta condición obstruye el flujo de orina desde la pelvis renal hacia el uréter, resultando en hidronefrosis y daño renal. El manejo principal de la UPO es quirúrgico. La pieloplastia es el tratamiento estándar para reconstruir la unión ureteropiélica y prevenir complicaciones. El artículo revisa un caso clínico de UPO extrínseca debido a una banda fibrosa, detallando síntomas, diagnóstico y el éxito del tratamiento quirúrgico. Masculino de 11 años sin antecedentes relevantes previ

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Pan, Bixia, Guohui Liu, Zongpei Jiang, and Dongwen Zheng. "Regulation of Renal Fibrosis by Macrophage Polarization." Cellular Physiology and Biochemistry 35, no. 3 (2015): 1062–69. http://dx.doi.org/10.1159/000373932.

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Background/Aims: Since renal fibrosis always predisposes end-stage renal disease, elucidation of the molecular mechanisms that underlie the progression of renal fibrosis may substantially improve the understanding and treatment for renal failure. Previous studies have highlighted an important counteraction between transforming growth factor β 1 (TGFβ1) and bone morphogenic protein 7 (BMP7) in the epithelial-to-mesenchymal transition (EMT) of renal tubular epithelial cells during chronic renal injury. Macrophages are also believed to play a critical role in renal fibrosis. However, the relation

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Lee, SW, AK Elfadl, MJ Chung, et al. "Urocystitis, pyelonephritis, renal papillary necrosis and chronic tubulointerstitial disease causing chronic renal insufficiency in a Siberian tiger (Panthera tigris altaica): a case report." Veterinární Medicína 63, No. 10 (2018): 482–87. http://dx.doi.org/10.17221/132/2017-vetmed.

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The present case report describes a case of chronic renal failure characterised by renal medullary fibrosis and renal papillary necrosis in a male Siberian tiger (Panthera tigris altaica). A 12-year-old male Siberian tiger presented with depression, anorexia and weight loss. Blood urea nitrogen (&gt; 50.4 mmol/l) and ammonia (71.7 µmol/l) were increased, suggesting chronic renal failure and uraemia. The tiger died secondary to gastric haemorrhage. At necropsy, the kidneys had yellow lesions in the medulla and renal papillae and petechiae in the cortex. The stomach had multiple mucosal ulce

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Hou, Huixian, Mai Horikawa, Yuki Narita, et al. "Suppression of Indoxyl Sulfate Accumulation Reduces Renal Fibrosis in Sulfotransferase 1a1-Deficient Mice." International Journal of Molecular Sciences 24, no. 14 (2023): 11329. http://dx.doi.org/10.3390/ijms241411329.

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Renal fibrosis is the final manifestation of chronic kidney disease (CKD); its prevention is vital for controlling CKD progression. Indoxyl sulfate (IS), a typical sulfate-conjugated uremic solute, is produced in the liver via the enzyme sulfotransferase (SULT) 1A1 and accumulates significantly during CKD. We investigated the toxicopathological role of IS in renal fibrosis using Sult1a1-KO mice and the underlying mechanisms. The unilateral ureteral obstruction (UUO) model was created; kidney IS concentrations, inflammation, and renal fibrosis were assessed on day 14. After UUO treatment, infla

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Liu, Xiaoming, Huijuan Wang, Kai Wang, and Ying Liu. "Targeting interferon-stimulated gene of 20 kDa protein (Isg20) inhibits ribosome biogenesis to ameliorate the progression of renal fibrosis." PLOS One 20, no. 7 (2025): e0322639. https://doi.org/10.1371/journal.pone.0322639.

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Chronic kidney disease (CKD) is a global health issue that significantly threatens human health, with its incidence increasing annually. Renal fibrosis is characterized by the progressive loss of kidney function, leading to significant morbidity and mortality. Although ribosome biogenesis has been reported to be increased in several kidney diseases, its role in renal fibrosis remains unclear. This study investigates the role of the interferon-stimulated gene of 20 kDa protein (Isg20), an RNA exonuclease involved in several stages of ribosome biogenesis, in the progression of renal fibrosis. Bi

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Ramani, Kritika, Dong Zhou, Roderick Tan, Youhua Liu, Sarah Gaffen, and Partha Sarathi Biswas. "Disruption of Interleukin-17 receptor A (IL-17RA) gene in mice aggravates renal interstitial fibrosis in obstructive nephropathy." Journal of Immunology 196, no. 1_Supplement (2016): 51.24. http://dx.doi.org/10.4049/jimmunol.196.supp.51.24.

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Abstract Renal fibrosis is the final outcome of obstructive nephropathy and a major cause of chronic renal failure. Renal fibrosis results from an imbalance between extracellular matrix (ECM) synthesis and degradation, which is regulated by multiple inflammatory mediators in the kidney. Recently, Interleukin-17 (IL-17) emerged as a key cytokine in lung and liver fibrosis. Although IL-17 producing cells were detected in the obstructed kidney, the role of IL-17 in renal fibrosis is unknown. We sought to define the contribution of IL-17 in renal fibrosis in obstructive nephropathy. Mice deficient

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Zhang, Wanfen, Xiaoping Li, Yushang Tang, Cheng Chen, Ran Jing, and Tongqiang Liu. "miR-155-5p Implicates in the Pathogenesis of Renal Fibrosis via Targeting SOCS1 and SOCS6." Oxidative Medicine and Cellular Longevity 2020 (June 8, 2020): 1–11. http://dx.doi.org/10.1155/2020/6263921.

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Renal fibrosis is associated with the reduction in the functional renal parenchyma and in most cases progresses to end-stage kidney failure, a devastating condition that requires lifelong dialysis or kidney transplantation. However, due to the extreme complexity in the pathogenesis of renal fibrosis and our limited knowledge, therapeutic options for renal fibrosis in the clinical setting are still scarce and often ineffective. Hence, further studies on the molecular mechanisms underlying renal fibrosis are compellingly needed. Multiple miRNAs have demonstrated to participate in kidney diseases

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Kim, Kristin P., Caitlin E. Williams, and Christopher A. Lemmon. "Cell–Matrix Interactions in Renal Fibrosis." Kidney and Dialysis 2, no. 4 (2022): 607–24. http://dx.doi.org/10.3390/kidneydial2040055.

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Renal fibrosis is a hallmark of end-stage chronic kidney disease. It is characterized by increased accumulation of extracellular matrix (ECM), which disrupts cellular organization and function within the kidney. Here, we review the bi-directional interactions between cells and the ECM that drive renal fibrosis. We will discuss the cells involved in renal fibrosis, changes that occur in the ECM, the interactions between renal cells and the surrounding fibrotic microenvironment, and signal transduction pathways that are misregulated as fibrosis proceeds. Understanding the underlying mechanisms o

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Cao, Yu-Han, Lin-Li Lv, Xu Zhang, et al. "Urinary vimentin mRNA as a potential novel biomarker of renal fibrosis." American Journal of Physiology-Renal Physiology 309, no. 6 (2015): F514—F522. http://dx.doi.org/10.1152/ajprenal.00449.2014.

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Renal fibrosis is a histological outcome of chronic kidney disease (CKD) progression. However, the noninvasive detection of renal fibrosis remains a challenge. Here we constructed a renal fibrosis target mRNA array and used it to detect urinary mRNAs of CKD patients for investigating potential noninvasive biomarkers of renal fibrosis. We collected urine samples from 39 biopsy-proven CKD patients and 11 healthy controls in the training set. Urinary mRNA profiles of 86 genes showed a total of 21 mRNAs that were differentially expressed between CKD patients and controls ( P < 0.05), and viment

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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 (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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Sugiura, Hidekazu, Takumi Yoshida, Shunji Shiohira, et al. "Reduced Klotho expression level in kidney aggravates renal interstitial fibrosis." American Journal of Physiology-Renal Physiology 302, no. 10 (2012): F1252—F1264. http://dx.doi.org/10.1152/ajprenal.00294.2011.

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Renal expression of the klotho gene is markedly suppressed in chronic kidney disease (CKD). Since renal fibrosis is the final common pathology of CKD, we tested whether decreased Klotho expression is a cause and/or a result of renal fibrosis in mice and cultured renal cell lines. We induced renal fibrosis by unilateral ureteral obstruction (UUO) in mice with reduced Klotho expression ( kl/+ mice) and compared them with wild-type mice. The UUO kidneys from kl/+ mice expressed significantly higher levels of fibrosis markers such as α-smooth muscle actin (α-SMA), fibronectin, and transforming gro

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Ding, Hao, Lei Jiang, Jing Xu, et al. "Inhibiting aerobic glycolysis suppresses renal interstitial fibroblast activation and renal fibrosis." American Journal of Physiology-Renal Physiology 313, no. 3 (2017): F561—F575. http://dx.doi.org/10.1152/ajprenal.00036.2017.

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Chronic kidney diseases generally lead to renal fibrosis. Despite great progress having been made in identifying molecular mediators of fibrosis, the mechanism that governs renal fibrosis remains unclear, and so far no effective therapeutic antifibrosis strategy is available. Here we demonstrated that a switch of metabolism from oxidative phosphorylation to aerobic glycolysis (Warburg effect) in renal fibroblasts was the primary feature of fibroblast activation during renal fibrosis and that suppressing renal fibroblast aerobic glycolysis could significantly reduce renal fibrosis. Both gene an

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Sun, Donglin, Jing Guo, Weifei Liang, Yangxiao Chen, Xiangqiu Chen, and Li Wang. "Anlotinib Alleviates Renal Fibrosis via Inhibition of the ERK and AKT Signaling Pathways." Oxidative Medicine and Cellular Longevity 2023 (February 18, 2023): 1–11. http://dx.doi.org/10.1155/2023/1686804.

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Purpose. We examined whether anlotinib can attenuate folic acid-induced and unilateral ureteral obstruction-induced renal fibrosis and explored the underlying antifibrotic mechanism. Materials and Methods. We have evaluated the effects of anlotinib on folic acid-induced and unilateral ureteral obstruction-induced renal fibrosis in mice through in vivo experiments of unilateral ureteral obstruction or folic acid-induced interstitial fibrosis and in vitro models of transforming growth factor-β1 induced HK-2 human renal proximal tubule cells. Serum renal function parameters and inflammatory cytok

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Cao, Yuhan, Yuwei Wang, Yinhua Liu, et al. "Decreased Expression of Urinary Mammalian Target of Rapamycin mRNA Is Related to Chronic Renal Fibrosis in IgAN." Disease Markers 2019 (August 14, 2019): 1–10. http://dx.doi.org/10.1155/2019/2424751.

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Background. Renal fibrosis is a common outcome of all pathological types of chronic kidney disease (CKD). However, the noninvasive detection of renal fibrosis remains a challenge. Methods. We collected urine samples from 154 biopsy-proven IgA nephropathy (IgAN) patients and 61 healthy controls. The expression of mTOR was measured and the correlation with renal function parameter and pathological indicators. The receiver operating characteristic (ROC) curve for the diagnosis of IgAN and renal fibrosis was calculated. Results. The urinary mammalian target of rapamycin (mTOR) expression was decre

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Lusiana, Evi, and Legiran Legiran. "Potential therapy of umbilical cord mesenchymal stem cells (UC-MSC) in renal fibrosis." Sains Medika: Jurnal Kedokteran dan Kesehatan 14, no. 1 (2023): 28. http://dx.doi.org/10.30659/sainsmed.v14i1.22458.

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Renal fibrosis (RF) is a severe kidney pathology defined by myofibroblast anomalies that create extracellular material on the interstitial and glomerular surfaces. The current therapy for treating renal disease has not achieved excellent results. A new theory about applying umbilical cord mesenchymal stem cells (UC-MSC) to treat renal fibrosis and other fibrosis-affected organs has been developed. This review aims to elucidate the role of UC-MSC in the therapy of renal fibrosis and summarize the numerous biological mechanisms involved. A search was undertaken using PubMed and Google Scholar fr

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Pan, Shengyu, Tianhui Yuan, Yuqi Xia, Weimin Yu, Xiangjun Zhou, and Fan Cheng. "Role of Histone Modifications in Kidney Fibrosis." Medicina 60, no. 6 (2024): 888. http://dx.doi.org/10.3390/medicina60060888.

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Chronic kidney disease (CKD) is characterized by persistent kidney dysfunction, ultimately resulting in end-stage renal disease (ESRD). Renal fibrosis is a crucial pathological feature of CKD and ESRD. However, there is no effective treatment for this condition. Despite the complex molecular mechanisms involved in renal fibrosis, increasing evidence highlights the crucial role of histone modification in its regulation. The reversibility of histone modifications offers promising avenues for therapeutic strategies to block or reverse renal fibrosis. Therefore, a comprehensive understanding of th

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Zhao, Jinfeng, Yue Guan, Yingxiu Jia, Yinghua Chen, and Yue Cai. "Aerobic exercise up-regulates Klotho to improve renal fibrosis associated with aging and its mechanism." PLOS ONE 19, no. 9 (2024): e0311055. http://dx.doi.org/10.1371/journal.pone.0311055.

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Renal fibrosis is a major cause of renal dysfunction and is a common pathological event in almost all forms of chronic kidney disease (CKD). Currently, the pathomechanisms of renal fibrosis are not well understood. However, researchers have demonstrated that aerobic exercise can improve renal fibrosis. Klotho is considered to be a negative regulator of renal fibrosis. In this study, we aimed to investigate the role and mechanism of Klotho in the improvement of renal fibrosis through aerobic exercise. We performed a 12-week aerobic exercise intervention in 19-month-old male C57BL/6J mice. Physi

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Zhang, Mingkang, Ruirui Cui, Yan Zhou та ін. "Accumulation of Renal Fibrosis in Hyperuricemia Rats Is Attributed to the Recruitment of Mast Cells, Activation of the TGF-β1/Smad2/3 Pathway, and Aggravation of Oxidative Stress". International Journal of Molecular Sciences 24, № 13 (2023): 10839. http://dx.doi.org/10.3390/ijms241310839.

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Renal fibrosis is relentlessly progressive and irreversible, and a life-threatening risk. With the continuous intake of a high-purine diet, hyperuricemia has become a health risk factor in addition to hyperglycemia, hypertension, and hyperlipidemia. Hyperuricemia is also an independent risk factor for renal interstitial fibrosis. Numerous studies have reported that increased mast cells (MCs) are closely associated with kidney injury induced by different triggering factors. This study investigated the effect of MCs on renal injury in rats caused by hyperuricemia and the relationship between MCs

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Bülow, Roman David, and Peter Boor. "Extracellular Matrix in Kidney Fibrosis: More Than Just a Scaffold." Journal of Histochemistry & Cytochemistry 67, no. 9 (2019): 643–61. http://dx.doi.org/10.1369/0022155419849388.

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Kidney fibrosis is the common histological end-point of progressive, chronic kidney diseases (CKDs) regardless of the underlying etiology. The hallmark of renal fibrosis, similar to all other organs, is pathological deposition of extracellular matrix (ECM). Renal ECM is a complex network of collagens, elastin, and several glycoproteins and proteoglycans forming basal membranes and interstitial space. Several ECM functions beyond providing a scaffold and organ stability are being increasingly recognized, for example, in inflammation. ECM composition is determined by the function of each of the

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

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Farris, Alton B., and Robert B. Colvin. "Renal interstitial fibrosis." Current Opinion in Nephrology and Hypertension 21, no. 3 (2012): 289–300. http://dx.doi.org/10.1097/mnh.0b013e3283521cfa.

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Wang, Yashu, Xinna Deng, Jinying Wei та ін. "Irisin ameliorates UUO-induced renal interstitial fibrosis through TGF-β1/periostin/MMP-2 signaling pathway". PLOS ONE 19, № 6 (2024): e0299389. http://dx.doi.org/10.1371/journal.pone.0299389.

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Renal fibrosis is the most common pathway in progressive kidney diseases. The unilateral ureteral obstruction (UUO) model is used to induce progressive renal fibrosis. We evaluated the effects of irisin on renal interstitial fibrosis in UUO mice. The GSE121190, GSE36496, GSE42303, and GSE96101 datasets were downloaded from the Gene Expression Omnibus (GEO) database. In total, 656 differentially expressed genes (DEGs) were identified in normal and UUO mouse renal samples. Periostin and matrix metalloproteinase-2 (MMP-2) were selected to evaluate the effect of irisin on renal fibrosis in UUO mic

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Sun, Qinxue, Maike Baues, Barbara M. Klinkhammer, et al. "Elastin imaging enables noninvasive staging and treatment monitoring of kidney fibrosis." Science Translational Medicine 11, no. 486 (2019): eaat4865. http://dx.doi.org/10.1126/scitranslmed.aat4865.

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Fibrosis is the common endpoint and currently the best predictor of progression of chronic kidney diseases (CKDs). Despite several drawbacks, biopsies remain the only available means to specifically assess the extent of renal fibrosis. Here, we show that molecular imaging of the extracellular matrix protein elastin allows for noninvasive staging and longitudinal monitoring of renal fibrosis. Elastin was hardly expressed in healthy mouse, rat, and human kidneys, whereas it was highly up-regulated in cortical, medullar, and perivascular regions in progressive CKD. Compared to a clinically releva

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Sang, Yizhen, Kenji Tsuji, Kazuhiko Fukushima, Kensaku Takahashi, Shinji Kitamura, and Jun Wada. "Semaporin3A inhibitor ameliorates renal fibrosis through the regulation of JNK signaling." American Journal of Physiology-Renal Physiology 321, no. 6 (2021): F740—F756. http://dx.doi.org/10.1152/ajprenal.00234.2021.

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Renal fibrosis is the common pathological pathway in the progression of renal diseases. This study, using a unilateral ureteral obstruction (UUO) mouse model, indicated increased semaphorin3A (SEMA3A) signaling in renal tubular cells as well as fibroblast cells under UUO surgery, and SEMA3A inhibitor ameliorated UUO-induced renal fibrosis through the regulation of JNK signaling. The study proposes the potential therapeutic option of SEMA3A inhibitor to treat renal fibrosis.

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