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Profibrotic pathways

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https://www.readbyqxmd.com/read/29115435/human-umbilical-cord-mesenchymal-stem-cells-alleviate-interstitial-fibrosis-and-cardiac-dysfunction-in-a-dilated-cardiomyopathy-rat-model-by-inhibiting-tnf%C3%A2-%C3%AE-and-tgf%C3%A2-%C3%AE-1-erk1-2-signaling-pathways
#1
Changyi Zhang, Guichi Zhou, Yezeng Chen, Sizheng Liu, Fen Chen, Lichun Xie, Wei Wang, Yonggang Zhang, Tianyou Wang, Xiulan Lai, Lian Ma
Dilated cardiomyopathy (DCM) is a disease of the heart characterized by pathological remodeling, including patchy interstitial fibrosis and degeneration of cardiomyocytes. In the present study, the beneficial role of human umbilical cord‑derived mesenchymal stem cells (HuMSCs) derived from Wharton's jelly was evaluated in the myosin‑induced rat model of DCM. Male Lewis rats (aged 8‑weeks) were injected with porcine myosin to induce DCM. Cultured HuMSCs (1x106 cells/rat) were intravenously injected 28 days after myosin injection and the effects on myocardial fibrosis and the underlying signaling pathways were investigated and compared with vehicle‑injected and negative control rats...
October 26, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29111086/role-of-interleukin-17-in-tgf-%C3%AE-signaling-mediated-renal-interstitial-fibrosis
#2
Bin Sun, Hui Wang, Lu Zhang, Xiaofan Yang, Mingshun Zhang, Xingxing Zhu, Xiaohui Ji, Huijuan Wang
BACKGROUND: Several studies suggest IL-17 is involved in the pathogenesis of organ fibrosis. The exact role of IL-17 in renal interstitial fibrosis has not been fully elucidated. METHODS: We compared the histopathology of renal fibrosis as well as profibrotic TGF-β signaling in wild-type (WT) and IL-17 knock-out (IL-17(-/-)) mice using UUO as the disease model. To find out the possible mechanisms involved in the exacerbated renal fibrosis happened to IL-17(-/-) mice, we analyzed the pattern of ECM synthesis by different fibroblasts cultured with IL-17 and associated signaling mediators...
October 27, 2017: Cytokine
https://www.readbyqxmd.com/read/29101170/the-prorenin-receptor-in-the-cardiovascular-system-and-beyond
#3
Matthew T Hennrikus, Alexis A Gonzalez, Minolfa C Prieto
Since the prorenin receptor (PRR) was first reported, investigations into its role in many cellular processes have been underway. Renin and prorenin binding to PRR and its soluble form (sPRR) increases angiotensin I formation and intracellular pathways resulting in induction of profibrotic factors. The PRR has supplementary roles as a vital accessory protein of the vacuolar-type H+-ATPase and also as an intermediate in Wnt signaling. As a component of the H-ATPase, the PRR has been found upregulated during cardiac stress...
November 3, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/29093267/loss-of-mir-141-200c-ameliorates-hepatic-steatosis-and-inflammation-by-reprogramming-multiple-signaling-pathways-in-nash
#4
Melanie Tran, Sang-Min Lee, Dong-Ju Shin, Li Wang
Accumulation of lipid droplets and inflammatory cell infiltration is the hallmark of nonalcoholic steatohepatitis (NASH). The roles of noncoding RNAs in NASH are less known. We aim to elucidate the function of miR-141/200c in diet-induced NASH. WT and miR-141/200c-/- mice were fed a methionine and choline deficient (MCD) diet for 2 weeks to assess markers of steatosis, liver injury, and inflammation. Hepatic miR-141 and miR-200c RNA levels were highly induced in human patients with NASH fatty liver and in WT MCD mice...
November 2, 2017: JCI Insight
https://www.readbyqxmd.com/read/29080401/reactive-oxygen-species-as-signaling-molecules-in-the-development-of-lung-fibrosis
#5
REVIEW
Francisco J Gonzalez-Gonzalez, Navdeep Chandel, Manu Jain, G R Scott Budinger
Pulmonary fibrosis is a relatively rare but devastating disease characterized by the excessive deposition of extracellular matrix. The increased matrix results in reduced lung compliance and increased work of breathing, while the obliteration of alveolar-capillary structures can result in hypoxemia and pulmonary hypertension, which manifests clinically as worsening shortness of breath, respiratory failure, and death. Unbiased genome-wide association studies combined with animal models suggest that damage to the alveolar epithelium is the initiating factor in pulmonary fibrosis...
October 10, 2017: Translational Research: the Journal of Laboratory and Clinical Medicine
https://www.readbyqxmd.com/read/29073967/inhibition-of-glycogen-synthase-kinase-3%C3%AE-blocks-mesomesenchymal-transition-and-attenuates-streptococcus-pneumonia-mediated-pleural-injury-in-mice
#6
Jake Boren, Grant Shryock, Alexis Fergis, Ann Jeffers, Shuzi Owens, Wenyi Qin, Kathleen B Koenig, Yoshikazu Tsukasaki, Satoshi Komatsu, Mitsuo Ikebe, Steven Idell, Torry A Tucker
Pleural loculation affects about 30,000 patients annually in the United States and in severe cases can resolve with restrictive lung disease and pleural fibrosis. Pleural mesothelial cells contribute to pleural rind formation by undergoing mesothelial mesenchymal transition (MesoMT), whereby they acquire a profibrotic phenotype characterized by increased expression of α-smooth muscle actin and collagen 1. Components of the fibrinolytic pathway (urokinase plasminogen activator and plasmin) are elaborated in pleural injury and strongly induce MesoMT in vitro...
November 2017: American Journal of Pathology
https://www.readbyqxmd.com/read/29068765/mechanisms-of-renal-fibrosis
#7
Benjamin D Humphreys
Tubulointerstitial fibrosis is a chronic and progressive process affecting kidneys during aging and in chronic kidney disease (CKD), regardless of cause. CKD and renal fibrosis affect half of adults above age 70 and 10% of the world's population. Although no targeted therapy yet exists to slow renal fibrosis, a number of important recent advances have clarified the cellular and molecular mechanisms underlying the disease. In this review, I highlight these advances with a focus on cells and pathways that may be amenable to therapeutic targeting...
October 25, 2017: Annual Review of Physiology
https://www.readbyqxmd.com/read/29066712/activation-of-stat3-integrates-common-profibrotic-pathways-to-promote-fibroblast-activation-and-tissue-fibrosis
#8
Debomita Chakraborty, Barbora Šumová, Tatjana Mallano, Chih-Wei Chen, Alfiya Distler, Christina Bergmann, Ingo Ludolph, Raymund E Horch, Kolja Gelse, Andreas Ramming, Oliver Distler, Georg Schett, Ladislav Šenolt, Jörg H W Distler
Signal transducer and activator of transcription 3 (STAT3) is phosphorylated by various kinases, several of which have been implicated in aberrant fibroblast activation in fibrotic diseases including systemic sclerosis (SSc). Here we show that profibrotic signals converge on STAT3 and that STAT3 may be an important molecular checkpoint for tissue fibrosis. STAT3 signaling is hyperactivated in SSc in a TGFβ-dependent manner. Expression profiling and functional studies in vitro and in vivo demonstrate that STAT3 activation is mediated by the combined action of JAK, SRC, c-ABL, and JNK kinases...
October 24, 2017: Nature Communications
https://www.readbyqxmd.com/read/29066090/genetic-variants-associated-with-susceptibility-to-idiopathic-pulmonary-fibrosis-in-people-of-european-ancestry-a-genome-wide-association-study
#9
Richard J Allen, Joanne Porte, Rebecca Braybrooke, Carlos Flores, Tasha E Fingerlin, Justin M Oldham, Beatriz Guillen-Guio, Shwu-Fan Ma, Tsukasa Okamoto, Alison E John, Ma'en Obeidat, Ivana V Yang, Amanda Henry, Richard B Hubbard, Vidya Navaratnam, Gauri Saini, Norma Thompson, Helen L Booth, Simon P Hart, Mike R Hill, Nik Hirani, Toby M Maher, Robin J McAnulty, Ann B Millar, Philip L Molyneaux, Helen Parfrey, Doris M Rassl, Moira K B Whyte, William A Fahy, Richard P Marshall, Eunice Oballa, Yohan Bossé, David C Nickle, Don D Sin, Wim Timens, Nick Shrine, Ian Sayers, Ian P Hall, Imre Noth, David A Schwartz, Martin D Tobin, Louise V Wain, R Gisli Jenkins
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease with high mortality, uncertain cause, and few treatment options. Studies have identified a significant genetic risk associated with the development of IPF; however, mechanisms by which genetic risk factors promote IPF remain unclear. We aimed to identify genetic variants associated with IPF susceptibility and provide mechanistic insight using gene and protein expression analyses. METHODS: We used a two-stage approach: a genome-wide association study in patients with IPF of European ancestry recruited from nine different centres in the UK and controls selected from UK Biobank (stage 1) matched for age, sex, and smoking status; and a follow-up of associated genetic variants in independent datasets of patients with IPF and controls from two independent US samples from the Chicago consortium and the Colorado consortium (stage 2)...
November 2017: Lancet Respiratory Medicine
https://www.readbyqxmd.com/read/29062589/integration-of-canonical-and-noncanonical-pathways-in-tlr4-signaling-complex-regulation-of-the-wound-repair-program
#10
REVIEW
Paula J McKeown-Longo, Paul J Higgins
Significance: Chronic inflammation and maladaptive repair contribute to the development of fibrosis that negatively impacts quality of life and organ function. The toll-like receptor (TLR) system is a critical node in the tissue response to both exogenous (pathogen-associated) and endogenous (damage-associated) molecular pattern factors (PAMPs and DAMPs, respectively). The development of novel TLR ligand-, pathway-, and/or target gene-specific therapeutics may have clinical utility in the management of the exuberant inflammatory/fibrotic tissue response to injury without compromising the host defense to pathogens...
October 1, 2017: Advances in Wound Care
https://www.readbyqxmd.com/read/29049722/a-ppar-gamma-agonist-rosiglitazone-suppresses-fibrotic-response-in-human-pterygium-fibroblasts-by-modulating-the-p38-mapk-pathway
#11
Selikem Abla Nuwormegbe, Joon Hyung Sohn, Sun Woong Kim
Purpose: Fibroblast activation may play an important role in pterygium progression. Synthetic peroxisome proliferator-activated receptor γ (PPAR-γ) ligands have been shown to be effective antifibrotic agents against transforming growth factor β1 (TGF-β1) induced fibrosis in several tissues. We aimed to investigate the antifibrotic effects of the PPAR-γ ligand rosiglitazone in pterygium fibroblasts and the underlying mechanisms. Methods: Profibrotic activation was induced by TGF-β1 in primary cultured human pterygium fibroblasts and the effect of rosiglitazone treatment on α-smooth muscle actin (α-SMA), and extra cellular matrix proteins synthesis was detected by western blotting, real-time PCR, immunostaining, and flow cytometry...
October 1, 2017: Investigative Ophthalmology & Visual Science
https://www.readbyqxmd.com/read/29038968/anti-fibrotic-nintedanib-a-new-opportunity-for-systemic-sclerosis-patients
#12
REVIEW
Ana Catarina Duarte, Maria José Santos, Ana Cordeiro
Systemic sclerosis is a connective tissue disease characterized by progressive skin thickening and a wide spectrum of internal organ involvement. Pathogenesis includes vasculopathy, inflammation, and fibrosis. Although immunosuppressants such as cyclophosphamide and mycophenolate mofetil have shown some benefit in interstitial lung disease management, it is still a major cause of morbi-mortality in these patients. Therefore, there is a current need for new therapies. Here, we report a 65-year-old female patient with limited cutaneous systemic sclerosis, anti-topoisomerase-positive and extensive lung disease...
October 16, 2017: Clinical Rheumatology
https://www.readbyqxmd.com/read/29033929/immunity-and-fibrogenesis-the-role-of-th17-il-17-axis-in-hbv-and-hcv-induced-chronic-hepatitis-and-progression-to-cirrhosis
#13
REVIEW
Feliciano Chanana Paquissi
Cirrhosis is a common final pathway for most chronic liver diseases; representing an increasing burden worldwide and is associated with increased morbidity and mortality. Current evidence has shown that, after an initial injury, the immune response has a significant participation in the ongoing damage, and progression from chronic viral hepatitis (CVH) to cirrhosis, driving the activation and maintenance of main fibrogenic pathways. Among immune deregulations, those related to the subtype 17 of T helper lymphocytes (Th17)/interleukin-17 (IL-17) axis have been recognized as key immunopathological and prognostic elements in patients with CVH...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28986417/cell-specific-expression-of-runt-related-transcription-factor-2-contributes-to-pulmonary-fibrosis
#14
Carlo Mümmler, Olivier Burgy, Sarah Hermann, Kathrin Mutze, Andreas Günther, Melanie Königshoff
Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease with limited therapeutic options and unknown etiology. IPF is characterized by epithelial cell injury, impaired cellular crosstalk between epithelial cells and fibroblasts, and the formation of fibroblast foci with increased extracellular matrix deposition (ECM). We investigated the role of runt-related transcription factor 2 (RUNX2), a master regulator of bone development that has been linked to profibrotic signaling. RUNX2 expression was up-regulated in lung homogenates from patients with IPF and in experimental bleomycin-induced lung fibrosis...
October 6, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28965860/hepatic-stellate-cell-targeted-imatinib-nanomedicine-versus-conventional-imatinib-a-novel-strategy-with-potent-efficacy-in-experimental-liver-fibrosis
#15
Nesrine S El-Mezayen, Wessam F El-Hadidy, Wessam M El-Refaie, Th I Shalaby, Mahmoud M Khattab, Aiman S El-Khatib
Liver fibrosis is a global health problem without approved treatment. Imatinib inhibits two key profibrotic pathways; platelet-derived growth factor (PDGF) and transforming growth factor-beta (TGF-β) and thus can be used to treat liver fibrosis. However, conventional imatinib therapy is hampered by low concentration at target tissue and increased toxicity to other tissues especially heart, lung and liver. Since hepatic stellate cells (HSCs) are the main contributors to liver fibrosis pathogenesis and sole hepatic vitamin A (VA) storage cells, they can be actively targeted by coupling liposomes to VA...
September 28, 2017: Journal of Controlled Release: Official Journal of the Controlled Release Society
https://www.readbyqxmd.com/read/28959097/the-role-of-endoglin-in-myocardial-fibrosis
#16
REVIEW
Kou-Gi Shyu
Myocardial fibrosis is closely associated with heart failure because myocardial fibrosis may cause the loss of normal cardiac function. Endoglin is a homeodimeric membrane glycoprotein, a co-receptor of transforming growth factor-β1 (TGF-β1) and β3. Endoglin is a potent mediator of profibrotic effects of angiotensin II on cardiac fibroblasts and can modulate the effect of TGF-β1 on extracellular matrix synthesis. These data indicate that endoglin plays an important role in fibrogenesis in cardiac remodeling...
September 2017: Acta Cardiologica Sinica
https://www.readbyqxmd.com/read/28921394/combination-therapy-with-pirfenidone-plus-prednisolone-ameliorates-paraquat-induced-pulmonary-fibrosis
#17
Rokhsana Rasooli, Fatemeh Pourgholamhosein, Younes Kamali, Fatemeh Nabipour, Ali Mandegary
Pirfenidone is known to slow the decline in vital capacity and increase survival in idiopathic pulmonary fibrosis (IPF). Besides, administration of glucocorticoids, e.g., prednisolone has been the conventional strategy to the treatment of patients with this disease, although their efficacy is under debate. Since multiple coactivated pathways are involved in the pathogenesis of IPF, combination therapy is a foundation strategy to cover many more synergetic mechanisms and increase response. The aim of the present study was to compare the therapeutic efficacy of prednisolone plus pirfenidone with pirfenidone alone in PQ-induced lung fibrosis...
September 18, 2017: Inflammation
https://www.readbyqxmd.com/read/28903945/complement-c5a-receptors-c5l2-and-c5ar-in-renal-fibrosis
#18
Ina V Martin, Annika Bohner, Peter Boor, Erdenechimeg Shagdarsuren, Ute Raffetseder, Frank Lammert, Jürgen Floege, Tammo Ostendorf, Susanne N Weber
Complement factor C5a has two known receptors, C5aR mediating pro-inflammatory effects and C5L2, a potential C5a scavenger. We previously identified C5a/C5aR signaling as a potent profibrotic pathway in the kidney. Here we tested for the first time the role of C5L2 in renal fibrosis. In unilateral ureteral obstruction (UUO)-induced kidney fibrosis, the expression of C5aR and C5L2 increased similarly and gradually as fibrosis progressed and was particularly prominent in injured dilated tubules. Genetic deficiency of either C5aR or C5L2 significantly reduced UUO-induced tubular injury...
September 13, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/28890699/sphingosine-1-phosphate-signaling-as-a-target-in-hepatic-fibrosis-therapy
#19
REVIEW
Bárbara González-Fernández, Diana I Sánchez, Javier González-Gallego, María J Tuñón
Liver fibrosis is an excess production of extracellular matrix proteins as a result of chronic liver disease which leads to cell death and organ dysfunction. The key cells involved in fibrogenesis are resident hepatic stellate cells (HSCs) which are termed myofibroblasts after activation, acquiring contractile, proliferative, migratory and secretory capability. Sphingosine 1-phosphate (S1P) is a bioactive sphingolipid with well-established effects on angiogenesis, carcinogenesis and immunity. Accumulating evidence demonstrates that this metabolite is involved in the profibrotic inflammatory process through the regulation of pleiotropic cell responses, such as vascular permeability, leukocyte infiltration, cell survival, migration, proliferation and HSCs differentiation to myofibroblasts...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28886261/syndecan-2-attenuates-radiation-induced-pulmonary-fibrosis-and-inhibits-fibroblast-activation-by-regulating-pi3k-akt-rock-pathway-via-cd148
#20
Konstantin Tsoyi, Sarah G Chu, Nasly G Patino-Jaramillo, Julie Wilder, Julian Villalba, Melanie Doyle-Eisele, Jacob McDonald, Xiaoli Liu, Souheil El-Chemaly, Mark A Perrella, Ivan O Rosas
RATIONALE: Radiation-induced pulmonary fibrosis is a severe complication of patients treated with thoracic irradiation. We have previously shown that syndecan-2 reduces fibrosis by exerting alveolar epithelial cytoprotective effects. Here, we investigate whether syndecan-2 attenuates radiation-induced pulmonary fibrosis by inhibiting fibroblast activation. METHODS: C57BL/6 wild type (WT) mice and transgenic (TG) mice that overexpress human syndecan-2 in alveolar macrophages were exposed to 14 Gy whole thoracic radiation...
September 8, 2017: American Journal of Respiratory Cell and Molecular Biology
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