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Profibrotic pathway

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https://www.readbyqxmd.com/read/29438665/cartilage-intermediate-layer-protein-1-alleviates-pressure-overload-induced-cardiac-fibrosis-via-interfering-tgf-%C3%AE-1-signaling
#1
Cheng-Lin Zhang, Qian Zhao, Hui Liang, Xue Qiao, Jin-Yu Wang, Dan Wu, Li-Ling Wu, Li Li
Cardiac fibrosis is characterized by excessive deposition of extracellular matrix (ECM) proteins in the myocardium and results in decreased ventricular compliance and diastolic dysfunction. Cartilage intermediate layer protein-1 (CILP-1), a novel identified cardiac matricellular protein, is upregulated in most conditions associated with cardiac remodeling, however, whether CILP-1 is involved in pressure overload-induced fibrotic response is unknown. Here, we investigated whether CILP-1 was critically involved in the fibrotic remodeling induced by pressure overload...
February 10, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29427621/brg1-promotes-liver-fibrosis-via-activation-of-hepatic-stellate-cells
#2
Haijie Li, Jingqin Lan, Caishun Han, Kaixuan Guo, Guihua Wang, Junbo Hu, Jianping Gong, Xuelai Luo, Zhixin Cao
Liver fibrosis, an important health concern associated to chronic liver injury that provides a permissive environment for cancer development, is characterized by the persistent deposition of extracellular matrix components mainly derived from activated hepatic stellate cells (HSCs). Brg1, the core subunit of the SWI/SNF chromatin remodeling complex, has been proved to associated with nonalcoholic steatohepatitis which may progress to cirrhosis. Herein, we determined whether Brg1 regulates liver fibrosis and examined its mechanism by focusing on HSCs activation...
February 7, 2018: Experimental Cell Research
https://www.readbyqxmd.com/read/29417309/il-33-can-promote-the-process-of-pulmonary-fibrosis-by-inducing-the-imbalance-between-mmp-9-and-timp-1
#3
Liyan Wu, Zujin Luo, Jinxu Zheng, Peng Yao, Zhenyan Yuan, Xiaohong Lv, Jing Zhao, Min Wang
IL-33 played an important role in inflammatory diseases as evidenced by their high levels of expression in diseased tissues. Previous studies showed that IL-33/ST2L signal transduction pathway participated in epithelial-mesenchymal transition (EMT) of A549 cells. Cytokine IL-1β can increase the expression of MMPs by activating NF-kB. The excessive or inappropriate expression of MMP-9 may randomly and non-selectively destroy the extracellular matrix. TIMP-1 (tissue inhibitor of MMP-9) effects on ebb and flow of ECM by inhibiting activation of MMP-9...
February 7, 2018: Inflammation
https://www.readbyqxmd.com/read/29411011/activation-of-the-nfat-calcium-signaling-pathway-in-human-lamina-cribrosa-cells-in-glaucoma
#4
Mustapha Irnaten, Alexander Zhdanov, Deirdre Brennan, Thomas Crotty, Abbot Clark, Dmitri Papkovsky, Colm O'Brien
Purpose: Optic nerve cupping in glaucoma is characterized by remodeling of the extracellular matrix (ECM) and fibrosis in the lamina cribrosa (LC). We have previously shown that glaucoma LC cells express raised levels of ECM genes and have elevated intracellular calcium ([Ca2+]i). Raised [Ca2+]i is known to promote proliferation, activation, and contractility in fibroblasts via the calcineurin-NFAT (nuclear factor of activated T-cells) signaling pathway. In this study, we examine NFAT expression in normal and glaucoma LC cells, and investigate the effect of cyclosporin A (CsA, a known inhibitor of NFAT activity) on [Ca2+]i and ECM gene expression in normal and glaucoma LC cells...
February 1, 2018: Investigative Ophthalmology & Visual Science
https://www.readbyqxmd.com/read/29401161/the-cellular-response-of-keloids-and-hypertrophic-scars-to-botulinum-toxin-a-a-comprehensive-literature-review
#5
Evan Austin, Eugene Koo, Jared Jagdeo
BACKGROUND: Keloids and hypertrophic scars are conditions of pathologic scarring characterized by fibroblast hyperproliferation and excess collagen deposition. These conditions significantly impact patients by causing psychosocial, functional, and aesthetic distress. Current treatment modalities have limitations. Clinical evidence indicates that botulinum toxin A (BoNT-A) may prevent and treat keloids and hypertrophic scars. OBJECTIVE: To examine investigated cellular pathways involved in BoNT-A therapeutic modulation of keloids and hypertrophic scars...
February 2018: Dermatologic Surgery: Official Publication for American Society for Dermatologic Surgery [et Al.]
https://www.readbyqxmd.com/read/29375046/one-session-of-exercise-regulates-cathepsin-b-activity-in-the-livers-of-trained-and-untrained-rats
#6
A Wyczalkowska-Tomasik, B Czarkowska-Paczek, J Piekarczyk-Persa, M Zendzian-Piotrowska
Physical exercise causes adaptive changes, mainly in muscles, but it also influences other organs, including liver. Most changes are beneficial; however, strenuous exercise is a strong stressor, and it can result in splanchnic hypoperfusion with subsequent disturbances in liver homeostasis and energy. Cathepsin B is a protease linked to protein turnover and extracellular matrix degradation. It is also involved in autophagy and the activation of proinflammatory and profibrotic pathways. This study investigated the influences of one session of exercise and endurance training on the mRNA, protein level, and activity of cathepsin B in rat liver...
October 2017: Journal of Physiology and Pharmacology: An Official Journal of the Polish Physiological Society
https://www.readbyqxmd.com/read/29367207/non-alcoholic-steatohepatitis-pathogenesis-sublethal-hepatocyte-injury-as-a-driver-of-liver-inflammation
#7
REVIEW
Samar H Ibrahim, Petra Hirsova, Gregory J Gores
A subset of patients with non-alcoholic fatty liver disease develop an inflammatory condition, termed non-alcoholic steatohepatitis (NASH). NASH is characterised by hepatocellular injury, innate immune cell-mediated inflammation and progressive liver fibrosis. The mechanisms whereby hepatic inflammation occurs in NASH remain incompletely understood, but appear to be linked to the proinflammatory microenvironment created by toxic lipid-induced hepatocyte injury, termed lipotoxicity. In this review, we discuss the signalling pathways induced by sublethal hepatocyte lipid overload that contribute to the pathogenesis of NASH...
January 24, 2018: Gut
https://www.readbyqxmd.com/read/29355590/targeting-tgf-%C3%AE-signaling-for-the-treatment-of-fibrosis
#8
REVIEW
Andrea H Györfi, Alexandru E Matei, Jörg H W Distler
Transforming growth factor-β (TGF-β) is widely recognized as a core pathway of fibrosis. Inhibition of TGF-β signaling may thus offer potential for antifibrotic therapies. Long-term inhibition of TGF-β signaling at the level of its isoforms and receptors can be associated with unacceptable adverse effects. However, TGF-β regulates a myriad of intracellular signaling cascades to transmit its profibrotic effects and several of those pathways offer potential for pharmacologic intervention. Moreover, the multiple interactions of TGF-β with other profibrotic pathways also yielded candidates for therapeutic intervention...
January 17, 2018: Matrix Biology: Journal of the International Society for Matrix Biology
https://www.readbyqxmd.com/read/29351440/jq1-is-a-potential-therapeutic-option-for-copd-patients-with-agrin-overexpression
#9
Zhen Xiao, Jing Shu, Feng Zhou, Yong Han
Chronic Obstructive Pulmonary Disease (COPD) is one of the leading cause of morbidity and death worldwide. It is characterized by chronic pulmonary inflammation and obstructed airflow from the lungs. To date, there is no effective treatments for COPD. The activation of Agrin (AGRN) - YAP pathway can promote heart regeneration. Since Agrin can only induce mild cardiomyocyte (CM) proliferation compare to ERBB2 pathway activation, it might exert pleiotropic effects, such as mitigation of innate inflammation, immune response and fibrosis...
December 28, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29343447/altered-b-lymphocyte-homeostasis-and-functions-in-systemic-sclerosis
#10
REVIEW
Alexandra Forestier, Thomas Guerrier, Mathieu Jouvray, Jonathan Giovannelli, Guillaume Lefèvre, Vincent Sobanski, Carine Hauspie, Eric Hachulla, Pierre-Yves Hatron, Hélène Zephir, Patrick Vermersch, Myriam Labalette, David Launay, Sylvain Dubucquoi
Beyond the production of autoantibodies, B-cells are thought to play a role in systemic sclerosis (SSc) by secreting proinflammatory/profibrotic cytokines. B-cells are a heterogeneous population with different subsets distinguished by their phenotypes and cytokine production. Data about B-cell subsets, cytokine production and intracellular pathways leading to this production are scarce in SSc. The aim of our study was to describe B-cell homeostasis, activation, proliferation, cytokine production in B-cells and serum and B-cell intracellular signaling pathways in SSc...
January 14, 2018: Autoimmunity Reviews
https://www.readbyqxmd.com/read/29339038/curcumin-inhibits-tgf-%C3%AE-1-induced-connective-tissue-growth-factor-expression-through-the-interruption-of-smad2-signaling-in-human-gingival-fibroblasts
#11
Jung-Tsu Chen, Chen-Ying Wang, Min-Huey Chen
BACKGROUND/PURPOSE: Many fibrotic processes are associated with an increased level of transforming growth factor-β1 (TGF-β1). TGF-β1 can increase synthesis of matrix proteins and enhance secretion of protease inhibitors, resulting in matrix accumulation. Connective tissue growth factor (CTGF) is a downstream profibrotic effector of TGF-β1 and is associated with the fibrosis in several human organs. Curcumin has been applied to reduce matrix accumulation in fibrotic diseases. This study was aimed to evaluate whether curcumin could suppress TGF-β1-induced CTGF expression and its related signaling pathway involving in this inhibitory action in primary human gingival fibroblasts...
January 13, 2018: Journal of the Formosan Medical Association, Taiwan Yi Zhi
https://www.readbyqxmd.com/read/29321022/serum-metabolic-profiling-identified-a-distinct-metabolic-signature-in-patients-with-idiopathic-pulmonary-fibrosis-a-potential-biomarker-role-for-lysopc
#12
Barbara Rindlisbacher, Cornelia Schmid, Thomas Geiser, Cédric Bovet, Manuela Funke-Chambour
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a lethal lung disease of unknown etiology. Patients present loss of lung function, dyspnea and dry cough. Diagnosis requires compatible radiologic imaging and, in undetermined cases, invasive procedures such as bronchoscopy and surgical lung biopsy. The pathophysiological mechanisms of IPF are not completely understood. Lung injury with abnormal alveolar epithelial repair is thought to be a major cause for activation of profibrotic pathways in IPF...
January 10, 2018: Respiratory Research
https://www.readbyqxmd.com/read/29311148/protein-kinases-g-are-essential-downstream-mediators-of-the-antifibrotic-effects-of-sgc-stimulators
#13
Alexandru-Emil Matei, Christian Beyer, Andrea-Hermina Györfi, Alina Soare, Chih-Wei Chen, Clara Dees, Christina Bergmann, Andreas Ramming, Andreas Friebe, Franz Hofmann, Oliver Distler, Georg Schett, Jörg H W Distler
OBJECTIVES: Stimulators of soluble guanylate cyclase (sGC) are currently investigated in clinical trials for the treatment of fibrosis in systemic sclerosis (SSc). In this study, we aim to investigate the role of protein kinases G (PKG) as downstream mediators of sGC-cyclic guanosine monophosphate (cGMP) in SSc. METHODS: Mice with combined knockout of PKG1 and 2 were challenged with bleomycin and treated with the sGC stimulator BAY 41-2272. Fibroblasts were treated with BAY 41-2272 and with the PKG inhibitor KT 5823...
January 8, 2018: Annals of the Rheumatic Diseases
https://www.readbyqxmd.com/read/29310804/the-cytoskeletal-network-regulates-expression-of-the-profibrotic-genes-pai-1-and-ctgf-in-vascular-smooth-muscle-cells
#14
Rohan Samarakoon, Paul J Higgins
Vascular smooth muscle cells (VSMCs) are subject to changing hemodynamic stimuli that alter cytoskeletal dynamics, cellular architecture, and structure-associated signal transduction. Tensional stress, force application, and structural perturbations are sensed by VSMCs and impact the physiological as well as pathophysiological responses of the vasculature. Microtubule-targeting drugs provide useful tools to analyze cytoskeletal-associated signaling pathways and their linkages to pathological outcomes. Architecture-based controls on a subset of profibrotic genes commonly expressed in vascular disease are highlighted by their frequent induction in mechanically manipulated cells and with associated changes in cytoskeletal dynamics...
2018: Advances in Pharmacology
https://www.readbyqxmd.com/read/29287092/connective-tissue-growth-factor-dependent-collagen-gene-expression-induced-by-mas-agonist-ar234960-in-human-cardiac-fibroblasts
#15
Arunachal Chatterjee, John Barnard, Christine Moravec, Russell Desnoyer, Kalyan Tirupula, Sadashiva S Karnik
Perspectives on whether the functions of MAS, a G protein-coupled receptor, are beneficial or deleterious in the heart remain controversial. MAS gene knockout reduces coronary vasodilatation leading to ischemic injury. G protein signaling activated by MAS has been implicated in progression of adaptive cardiac hypertrophy to heart failure and fibrosis. In the present study, we observed increased expression of MAS, connective tissue growth factor (CTGF) and collagen genes in failing (HF) human heart samples when compared to non-failing (NF)...
2017: PloS One
https://www.readbyqxmd.com/read/29277328/induction-of-cytochrome-p450-4a14-contributes-to-angiotensin-ii-induced-renal-fibrosis-in-mice
#16
Yunfeng Zhou, Jingwei Yu, Jia Liu, Rong Cao, Wen Su, Sha Li, Shiqi Ye, Chenggang Zhu, Xiaolin Zhang, Hu Xu, Hua Chen, Xiaoyan Zhang, Youfei Guan
Angiotensin II (AngII) plays an important role in the pathogenesis of hypertension and associated renal injuries. To elucidate the molecular mechanism by which AngII induces renal damage, we found that AngII infusion significantly induced CYP4A14 expression in renal proximal tubule cells (RPTCs) with marked increases in blood pressure and proteinuria. Renal production of the major CYP4A metabolite, 20-HETE, was also significantly increased in the AngII-treated mice. Compared to wild-type (WT) mice, CYP4A14 knockout (CYP4A14-/-) mice exhibited significantly lower levels of blood pressure, renal 20-HETE production, proteinuria and renal fibrosis following AngII infusion...
December 19, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29215326/the-role-of-fabp5-in-radiation-induced-human-skin-fibrosis
#17
Jianyuan Song, Huojun Zhang, Zhenyu Wang, Wanglei Xu, Li Zhong, Jinming Cao, Jianfeng Yang, Ye Tian, Daojiang Yu, Jiang Ji, Jianping Cao, Shuyu Zhang
Radiation-induced skin fibrosis is a detrimental and chronic disorder that occurs after radiation exposure. The molecular changes underlying the pathogenesis of radiation-induced fibrosis of human skin have not been extensively reported. Technical advances in proteomics have enabled exploration of the biomarkers and molecular pathogenesis of radiation-induced skin fibrosis, with the potential to broaden our understanding of this disease. In this study, we compared protein expression in radiation-induced fibrotic human skin and adjacent normal tissues using iTRAQ-based proteomics technology...
December 7, 2017: Radiation Research
https://www.readbyqxmd.com/read/29214163/protective-effects-of-pyridoxamine-supplementation-in-the-early-stages-of-diet-induced-kidney-dysfunction
#18
F Chiazza, A S Cento, D Collotta, D Nigro, G Rosa, F Baratta, V Bitonto, J C Cutrin, M Aragno, R Mastrocola, M Collino
Pyridoxamine, a structural analog of vitamin B6 that exerts antiglycative effects, has been proposed as supplementary approach in patients with initial diabetic nephropathy. However, the molecular mechanism(s) underlying its protective role has been so far slightly examined. C57Bl/6J mice were fed with a standard diet (SD) or a diet enriched in fat and fructose (HD) for 12 weeks. After 3 weeks, two subgroups of SD and HD mice started pyridoxamine supplementation (150 mg/kg/day) in the drinking water. HD fed mice showed increased body weight and impaired glucose tolerance, whereas pyridoxamine administration significantly improved insulin sensitivity, but not body weight, and reduced diet-induced increase in serum creatinine and urine albumin...
2017: BioMed Research International
https://www.readbyqxmd.com/read/29193875/dabigatran-inhibits-intravitreal-thrombin-activity
#19
Jeroen Bastiaans, Verena C Mulder, Jan C van Meurs, Marja Smits-Te Nijenhuis, Conny van Holten-Neelen, P Martin van Hagen, Willem A Dik
PURPOSE: Proliferative vitreoretinopathy (PVR) is a vitreoretinal disorder in which retinal pigment epithelial (RPE) cell activation contributes to both formation of fibrotic retinal membranes and inflammation. Vitreous of patients with PVR contains increased thrombin activity which induces profibrotic and proinflammatory programs in RPE cells. Inhibition of intravitreal thrombin activity may thus represent a therapeutic option for PVR. In this study, we examined the capacity of the clinically available direct thrombin inhibitor dabigatran to inhibit thrombin activity in vitreous fluids...
November 30, 2017: Acta Ophthalmologica
https://www.readbyqxmd.com/read/29191563/tgf-%C3%AE-1-p53-signaling-in-renal-fibrogenesis
#20
Stephen P Higgins, Yi Tang, Craig E Higgins, Badar Mian, Wenzheng Zhang, Ralf-Peter Czekay, Rohan Samarakoon, David J Conti, Paul J Higgins
Fibrotic disorders of the renal, pulmonary, cardiac, and hepatic systems are associated with significant morbidity and mortality. Effective therapies to prevent or curtail the advancement to organ failure, however, remain a major clinical challenge. Chronic kidney disease, in particular, constitutes an increasing medical burden affecting >15% of the US population. Regardless of etiology (diabetes, hypertension, ischemia, acute injury, urologic obstruction), persistently elevated TGF-β1 levels are causatively linked to the activation of profibrotic signaling networks and disease progression...
November 28, 2017: Cellular Signalling
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