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Profibrotic pathway

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https://www.readbyqxmd.com/read/28424623/notch-signaling-in-ischemic-damage-and-fibrosis-evidence-and-clues-from-the-heart
#1
REVIEW
Silvia Nistri, Chiara Sassoli, Daniele Bani
Notch signaling is a major intercellular coordination mechanism highly conserved throughout evolution. In vertebrates, Notch signaling is physiologically involved in embryo development, including mesenchymal cell commitment, formation of heart tissues and angiogenesis. In post-natal life, Notch signaling is maintained as a key mechanism of cell-cell communication and its dysregulations have been found in pathological conditions such as ischemic and fibrotic diseases. In the heart, Notch takes part in the protective response to ischemia, being involved in pre- and post-conditioning, reduction of reperfusion-induced oxidative stress and myocardial damage, and cardiomyogenesis...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28409352/epithelial-to-mesenchymal-transition-emt-and-endothelial-to-mesenchymal-transition-endmt-role-and-implications-in-kidney-fibrosis
#2
Ana S Cruz-Solbes, Keith Youker
Tubulointerstitial injury is one of the hallmarks of renal disease. In particular, interstitial fibrosis has a prominent role in the development and progression of kidney injury. Collagen-producing fibroblasts are responsible for the ECM deposition. However, the origin of those activated fibroblasts is not clear. This chapter will discuss in detail the concept of epithelial to mesenchymal transition (EMT) and endothelial to mesenchymal transition (EndMT) in the context of fibrosis and kidney disease. In short, EMT and EndMT involve a change in cell shape, loss of polarity and increased motility associated with increased collagen production...
2017: Results and Problems in Cell Differentiation
https://www.readbyqxmd.com/read/28405618/efficacy-of-alk5-inhibition-in-myelofibrosis
#3
Lanzhu Yue, Matthias Bartenstein, Wanke Zhao, Wanting Tina Ho, Ying Han, Cem Murdun, Adam W Mailloux, Ling Zhang, Xuefeng Wang, Anjali Budhathoki, Kith Pradhan, Franck Rapaport, Huaquan Wang, Zonghong Shao, Xiubao Ren, Ulrich Steidl, Ross L Levine, Zhizhuang Joe Zhao, Amit Verma, Pearlie K Epling-Burnette
Myelofibrosis (MF) is a bone marrow disorder characterized by clonal myeloproliferation, aberrant cytokine production, extramedullary hematopoiesis, and bone marrow fibrosis. Although somatic mutations in JAK2, MPL, and CALR have been identified in the pathogenesis of these diseases, inhibitors of the Jak2 pathway have not demonstrated efficacy in ameliorating MF in patients. TGF-β family members are profibrotic cytokines and we observed significant TGF-β1 isoform overexpression in a large cohort of primary MF patient samples...
April 6, 2017: JCI Insight
https://www.readbyqxmd.com/read/28396839/inhibition-of-the-tgf%C3%AE-signalling-pathway-by-cgmp-and-cgmp-dependent-kinase-i-in-renal-fibrosis
#4
Elisabeth Schinner, Veronika Wetzl, Andrea Schramm, Frieder Kees, Peter Sandner, Johannes-Peter Stasch, Franz Hofmann, Jens Schlossmann
Agents that enhance production of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) ameliorate the progression of renal fibrosis. However, the molecular mechanism of this process is not fully understood. We hypothesize that the antifibrotic effects of cGMP and cGMP-dependent kinase I (cGKI) are mediated via regulation of the TGFβ signalling pathway, both via ERK and the Smad-dependent route. Kidney fibrosis was induced by unilateral ureter obstruction (UUO) in wild-type and cGKI-deficient (cGKI-KO) mice...
April 2017: FEBS Open Bio
https://www.readbyqxmd.com/read/28387853/cxcl8-antagonist-improves-diabetic-nephropathy-in-male-mice-of-diabetes-and-attenuates-high-glucose-induced-mesangial-injury
#5
Siyuan Cui, Yujie Zhu, Jianling Du, Muhammad Noman Khan, Bing Wang, Jing Wei, Jya-Wei Cheng, John R Gordon, Yutian Mu, Fang Li
Inflammation is recognized as a crucial contribution to diabetic nephropathy (DN). CXCL8 binds to its CXC chemokine receptors (CXCR1 and CXCR2) for recruiting neutrophils infiltration and initiates tissue inflammation. Therefore, we explored the effect of CXCR1 and CXCR2 inhibition on diabetic nephropathy. This was achieved by CXCL8 (3-72) K11R/G31P (G31P), an antagonist of CXCL8, which has exhibited therapeutic efficacy in inflammatory diseases and malignancies. In this study, we found renal leukocytes accumulation and rapid increases of CXCL8 occurred in HFD/STZ-induced diabetic mice...
April 6, 2017: Endocrinology
https://www.readbyqxmd.com/read/28382387/high-soluble-endoglin-levels-do-not-induce-changes-in-structural-parameters-of-mouse-heart
#6
Jana Rathouska, Petra Fikrova, Alena Mrkvicova, Katerina Blazickova, Michala Varejckova, Eva Dolezelova, Ivana Nemeckova, Barbora Vitverova, Lenka Peslova, Eunate Gallardo-Vara, Miguel Pericacho, Petr Nachtigal
A soluble form of endoglin (sEng) released into the circulation was suggested to be a direct inducer of endothelial dysfunction, inflammation and contributed to the development of hypertension by interfering with TGF-β signaling in cardiovascular pathologies. In the present study, we assessed the hypothesis that high sEng level-induced hypertension via a possible sEng interference with TGF-β signaling pathways may result in inflammatory, structural or fibrotic changes in hearts of Sol-Eng+ mice (mice with high levels of soluble endoglin) fed either chow or high-fat diet...
April 5, 2017: Heart and Vessels
https://www.readbyqxmd.com/read/28363295/biological-principles-of-scar-and-contracture
#7
REVIEW
Peter O Kwan, Edward E Tredget
Hypertrophic scar and contracture in burn patients is a complex process. Contributing factors include critical injury depth and activation of key cell subpopulations, including deep dermal fibroblasts, myofibroblasts, fibrocytes, and T-helper cells, which cause scarring rather than regeneration. These cells influence each other via cellular profibrotic and antifibrotic signals, which help to determine the outcome. These cells also both modify and interact with extracellular matrix of the wound, ultimately forming hypertrophic scar...
May 2017: Hand Clinics
https://www.readbyqxmd.com/read/28358366/forkhead-box-a3-attenuated-the-progression-of-fibrosis-in-a-rat-model-of-biliary-atresia
#8
Rui Dong, Yifan Yang, Zhen Shen, Chao Zheng, Zhu Jin, Yanlei Huang, Zhien Zhang, Shan Zheng, Gong Chen
Biliary atresia is a rare, devastating disease of infants where a fibroinflammatory process destroys the bile ducts, leading to fibrosis and biliary cirrhosis, and death if untreated. The cause and pathogenesis remain largely unknown. We tried to investigate factors involved in biliary atresia, especially forkhead box A3 (Foxa3), which might exert a role in the treatment of liver disease. We used RNA sequencing to sequence the whole transcriptomes of livers from six biliary atresia and six choledochal cysts patients...
March 30, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28337301/endoplasmic-reticulum-stress-a-new-wrestler-in-the-pathogenesis-of-idiopathic-pulmonary-fibrosis
#9
Lei Zhang, Yi Wang, Nuruliarizki Shinta Pandupuspitasari, Guorao Wu, Xudong Xiang, Quan Gong, Weining Xiong, Cong-Yi Wang, Ping Yang, Boxu Ren
Idiopathic pulmonary fibrosis (IPF) has attracted extensive attention for its unexplained progressive lung scarring, short median survival and its unresponsiveness to traditional therapies. Despite extensive studies, the mechanisms underlying IPF pathoetiologies, however, remain poorly understood. Recent advances delineated a potential function of endoplasmic reticulum (ER) stress in meeting the need of fibrotic response, which pinpointed a critical role for the unfolded protein response (UPR) pathways in IPF pathogenesis...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/28294324/blocking-fibrotic-signaling-in-fibroblasts-from-patients-with-carpal-tunnel-syndrome
#10
REVIEW
Yoshiaki Yamanaka, Anne Gingery, Gosuke Oki, Tai-Hua Yang, Chunfeng Zhao, Peter C Amadio
Fibrosis of the subsynovial connective tissue (SSCT) in carpal tunnel syndrome (CTS) patients is increasingly recognized as an important aspect of CTS pathophysiology. In this study, we evaluated the effect of blocking profibrotic pathways in fibroblasts from the SSCT in CTS patients. Fibroblasts were stimulated with transforming growth factor β1 (TGF-β1), and then treated either with a specific fibrosis pathway inhibitor targeting TGF-β receptor type 1 (TβRI), platelet-derived growth factor receptor (PDGFR), epidermal growth factor receptor (EGFR) or vascular endothelial growth factor receptor (VEGFR)...
March 10, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28284377/treatment-of-renal-fibrosis-turning-challenges-into-opportunities
#11
REVIEW
Barbara M Klinkhammer, Roel Goldschmeding, Jürgen Floege, Peter Boor
Current treatment modalities are not effective in halting the progression of most CKD. Renal fibrosis is a pathological process common to all CKD and thereby represents an excellent treatment target. A large number of molecular pathways involved in renal fibrosis were identified in preclinical studies, some of them being similar among different organs and some with available drugs in various phases of clinical testing. Yet only few clinical trials with antifibrotic drugs are being conducted in CKD patients...
March 2017: Advances in Chronic Kidney Disease
https://www.readbyqxmd.com/read/28283950/caveolin-1-in-the-pathogenesis-of-diabetic-nephropathy-potential-therapeutic-target
#12
REVIEW
Richard Van Krieken, Joan C Krepinsky
PURPOSE OF REVIEW: Diabetic nephropathy, a major microvascular complication of diabetes and the most common cause of end-stage renal disease, is characterized by prominent accumulation of extracellular matrix. The membrane microdomains caveolae, and their integral protein caveolin-1, play critical roles in the regulation of signal transduction. In this review we discuss current knowledge of the contribution of caveolin-1/caveolae to profibrotic signaling and the pathogenesis of diabetic kidney disease, and assess its potential as a therapeutic target...
March 2017: Current Diabetes Reports
https://www.readbyqxmd.com/read/28282408/the-renal-phenotype-of-allopurinol-treated-hprt-deficient-mouse
#13
Cristina Zennaro, Federica Tonon, Paola Zarattini, Milan Clai, Alessandro Corbelli, Michele Carraro, Marialaura Marchetti, Luca Ronda, Gianluca Paredi, Maria Pia Rastaldi, Riccardo Percudani
Excess of uric acid is mainly treated with xanthine oxidase (XO) inhibitors, also called uricostatics because they block the conversion of hypoxanthine and xanthine into urate. Normally, accumulation of upstream metabolites is prevented by the hypoxanthine-guanine phosphoribosyltransferase (HPRT) enzyme. The recycling pathway, however, is impaired in the presence of HPRT deficiency, as observed in Lesch-Nyhan disease. To gain insights into the consequences of purine accumulation with HPRT deficiency, we investigated the effects of the XO inhibitor allopurinol in Hprt-lacking (HPRT-/-) mice...
2017: PloS One
https://www.readbyqxmd.com/read/28274188/extracellular-matrix-remodeling-in-idiopathic-pulmonary-fibrosis-it-is-the-bed-that-counts-and-not-the-sleepers
#14
Ioannis P Tomos, Argyrios Tzouvelekis, Vassilis Aidinis, Effrosyni D Manali, Evangelos Bouros, Demosthenes Bouros, Spyros A Papiris
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive interstitial lung disease characterized by irreversible fibrosis. Current disease pathogenesis assumes an aberrant wound healing process in response to repetitive injurious stimuli leading to apoptosis of epithelial cells, activation of fibroblasts and accumulation of extracellular matrix (ECM). Particularly, lung ECM is a highly dynamic structure that lies at the core of several physiological and developmental pathways. The scope of this review article is to summarize current knowledge on the role of ECM in the pathogenesis of IPF, unravel novel mechanistic data and identify future more effective therapeutic targets...
March 8, 2017: Expert Review of Respiratory Medicine
https://www.readbyqxmd.com/read/28271726/molecular-mechanisms-of-atrial-fibrosis-implications-for-the-clinic
#15
REVIEW
Shivshankar Thanigaimani, Dennis H Lau, Thomas Agbaedeng, Adrian D Elliott, Rajiv Mahajan, Prashanthan Sanders
Recent research has unravelled an increasing list of cardiac conditions and risk factors that may be responsible for the abnormal underlying atrial substrate that predisposes to atrial fibrillation (AF). Atrial fibrosis has been demonstrated as the pivotal structural abnormality underpinning conduction disturbances that promote AF in different disease models. Despite the advancement in our discoveries of the molecular mechanisms involved in the profibrotic milieu, targeted therapeutics against atrial fibrosis remain lacking...
April 2017: Expert Review of Cardiovascular Therapy
https://www.readbyqxmd.com/read/28256533/myofibroblast-differentiation-and-its-functional-properties-are-inhibited-by-nicotine-and-e-cigarette-via-mitochondrial-oxphos-complex-iii
#16
Wei Lei, Chad Lerner, Isaac K Sundar, Irfan Rahman
Nicotine is the major stimulant in tobacco products including e-cigarettes. Fibroblast to myofibroblast differentiation is a key process during wound healing and is dysregulated in lung diseases. The role of nicotine and e-cigarette derived nicotine on cellular functions including profibrotic response and other functional aspects is not known. We hypothesized that nicotine and e-cigarettes affect myofibroblast differentiation, gel contraction, and wound healing via mitochondria stress through nicotinic receptor-dependent mechanisms...
March 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28253513/microarray-analysis-reveals-increased-expression-of-matrix-metalloproteases-and-cytokines-of-interleukin-20-subfamily-in-the-kidneys-of-neonate-rats-underwent-unilateral-ureteral-obstruction-a-potential-role-of-il-24-in-the-regulation-of-inflammation-and-tissue
#17
Domonkos Pap, Erna Sziksz, Zoltán Kiss, Réka Rokonay, Apor Veres-Székely, Rita Lippai, István Márton Takács, Éva Kis, Andrea Fekete, György Reusz, Adam Vannay, Attila J Szabó
BACKGROUND/AIMS: Congenital obstructive nephropathy (CON) is the main cause of pediatric chronic kidney diseases leading to renal fibrosis. High morbidity and limited treatment opportunities of CON urge the better understanding of the underlying molecular mechanisms. METHODS: To identify the differentially expressed genes, microarray analysis was performed on the kidney samples of neonatal rats underwent unilateral ureteral obstruction (UUO). Microarray results were then validated by real-time RT-PCR and bioinformatics analysis was carried out to identify the relevant genes, functional groups and pathways involved in the pathomechanism of CON...
February 28, 2017: Kidney & Blood Pressure Research
https://www.readbyqxmd.com/read/28249987/trpv4-ion-channel-is-a-novel-regulator-of-dermal-myofibroblast-differentiation
#18
Shweta Sharma, Rishov Goswami, Michael Merth, Jonathan Cohen, Kai Y Lei, David X Zhang, Shaik O Rahaman
Scleroderma is a multisystem fibroproliferative disease with no effective medical treatment. Myofibroblasts are critical to the fibrogenic tissue repair process in the skin and many internal organs. Emerging data support a role for both matrix stiffness, and transforming growth factor β1 (TGFβ1), in myofibroblast differentiation. Transient receptor potential vanilloid 4 (TRPV4) is a mechanosensitive ion channel activated by both mechanical and biochemical stimuli. The objective of this study was to determine the role of TRPV4 in TGFβ1- and matrix stiffness-induced differentiation of dermal fibroblasts...
March 1, 2017: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/28245135/connexin43-controls-the-myofibroblastic-differentiation-of-bronchial-fibroblasts-from-asthmatic-patients
#19
Milena Paw, Izabela Borek, Dawid Wnuk, Damian Ryszawy, Katarzyna Piwowarczyk, Katarzyna Kmiotek, Katarzyna A Wójcik-Pszczoła, Małgorzata Pierzchalska, Zbigniew Madeja, Marek Sanak, Przemysław Błyszczuk, Marta Michalik, Jarosław Czyż
Pathologic accumulation of myofibroblasts in asthmatic bronchi is regulated by extrinsic stimuli and by the intrinsic susceptibility of bronchial fibroblasts to transforming growth factor-β (TGF-β). The specific function of gap junctions and connexins in this process remained unknown. Here, we investigated the role of connexin (Cx)43 in TGF-β-induced myofibroblastic differentiation of fibroblasts derived from bronchoscopic biopsies of asthmatic patients and non-asthmatic donors. Asthmatic fibroblasts expressed considerably higher levels of Cx43 and were more susceptible to TGF-β1-induced myofibroblastic differentiation than their non-asthmatic counterparts...
February 28, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28240316/p53-induces-mir199a-3p-to-suppress-socs7-for-stat3-activation-and-renal-fibrosis-in-uuo
#20
Ruhao Yang, Xuan Xu, Huiling Li, Jinwen Chen, Xudong Xiang, Zheng Dong, Dongshan Zhang
The role of p53 in renal fibrosis has recently been suggested, however, its function remains controversial and the underlying mechanism is unclear. Here, we show that pharmacological and genetic blockade of p53 attenuated renal interstitial fibrosis, apoptosis, and inflammation in mice with unilateral urethral obstruction (UUO). Interestingly, p53 blockade was associated with the suppression of miR-215-5p, miR-199a-5p&3p, and STAT3. In cultured human kidney tubular epithelial cells (HK-2), TGF-β1 treatment induced fibrotic changes, including collagen I and vimentin expression, being associated with p53 accumulation, p53 Ser15 phosphorylation, and miR-199a-3p expression...
February 27, 2017: Scientific Reports
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