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Emerging immune functions of non-hematopoietic stromal cells

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193622 Year: Pages: 161 DOI: 10.3389/978-2-88919-362-2 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2015-11-19 16:29:12
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Abstract

The development and function of the immune system is dependent on interactions between haematopoietic cells and non-hematopoietic stromal cells. The non-hematopoietic stromal cells create the microenvironment in which the immune system operates, providing an architectural landscape for hematopoietic cell-cell interactions and molecular cues governing haematopoietic cell positioning, growth and survival. Not surprisingly, therefore, aberrant stromal cell function has recently been shown to play a key role in the development of disease pathologies associated with immune dysfunction. For example, remodelling of lymphoid tissue stroma and the development of ectopic tertiary lymphoid tissues are characteristic of many infectious and inflammatory diseases and stromal cells have a recognised role in lymphoma and tumour development and resistance to therapy. An increased understanding of the molecular basis of stromal cell differentiation and function in these varied contexts will provide new tools to promote research on stromal cell biology and immune dysfunction, and potential new targets for therapeutic intervention in diseases with a major impact on public health. The importance of stromal cells and the molecular mechanisms of stromal cell function in the regulation of immune responses have only recently been appreciated and thus represent an exciting new area in immunology.

Advances in Mechanisms of Renal Fibrosis

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889454990 Year: Pages: 84 DOI: 10.3389/978-2-88945-499-0 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Physiology
Added to DOAB on : 2019-01-23 14:53:42
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Scarring of the glomerular and tubulointerstitial compartments is a hallmark of progressive kidney disease. Renal fibrosis involves a complex interplay between kidney cells, leukocytes and fibroblasts in which transforming growth factor-β (TGF-β) plays a key role. This eBook provides a comprehensive update on TGF-β signalling pathways and introduces a range of cellular and molecular mechanisms involved in renal fibrosis both upstream and downstream of TGF-β. The wide variety of potential new targets described herein bodes well for the future development of effective therapies to tackle the major clinical problem of progressive renal fibrosis.

Keywords

BMP7 --- fibroblast --- HDAC --- HIPK2 --- JNK --- miRNA --- non-classical RAS --- Smad --- TGF-beta

Molecular Basis of Cardiovascular Diseases: Implications of Natriuretic Peptides

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ISBN: 9783039215829 / 9783039215836 Year: Pages: 212 DOI: 10.3390/books978-3-03921-583-6 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General) --- Cardiovascular
Added to DOAB on : 2019-12-09 11:49:16
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The natriuretic peptides (NPs) family includes a class of hormones and their receptors needed for the physiological control of cardiovascular functions. The discovery of NPs provided a fundamental contribution into our understanding of the physiological regulation of blood pressure, and of heart and kidney functions. NPs have also been implicated in the pathogenesis of several cardiovascular diseases (CVDs), including hypertension, atherosclerosis, heart failure, and stroke. A fine comprehension of the molecular mechanisms dependent from NPs and underlying the promotion of cardiovascular damage has contributed to improve our understanding of the molecular basis of all major CVDs. Finally, the opportunity to target NPs in order to develop new therapeutic tools for a better treatment of CVDs has been developed over the years. The current Special Issue of the Journal covers all major aspects of the molecular implications of NPs in physiology and pathology of the cardiovascular system, including NP-based therapeutic approaches.

Keywords

PCSK9 --- natriuretic peptides --- adipose tissue --- lipid metabolism --- LDL receptor --- insulin --- natriuretic peptides --- hypertension --- stroke --- cardiac hypertrophy --- linkage analysis --- genetic variants --- animal models --- BNP --- NT-proBNP --- heart failure --- cardiac dysfunction --- forensic medicine --- postmortem biochemistry --- angiotensin receptor–neprilysin inhibitor --- natriuretic peptides --- renin–angiotensin system --- heart failure --- arterial hypertension --- natriuretic peptide --- vascular --- endothelial cell --- cardiomyocyte --- fibroblast --- inflammation --- heart failure --- hypertension --- angiogenesis --- heart failure --- natriuretic peptides --- preserved ejection fraction --- natriuretic peptides --- heart failure --- atrial fibrillation --- remodeling --- Idiopathic Pulmonary Arterial Hypertension (IPAH) --- Natriuretic Peptide Clearance Receptor (NPR-C) signaling --- atrial natriuretic peptide --- hypertension --- heart failure --- cardiometabolic disease --- obesity --- metabolic syndrome --- cGMP --- guanylyl cyclase receptor A --- natriuretic peptides --- natriuretic peptide --- cardiorenal syndrome --- vasopressor --- vasodilator --- kidney --- medulla --- renin-angiotensin-aldosterone system --- Atrial Natriuretic peptide --- natriuretic peptides --- cardiac remodelling --- cardiac hypertrophy --- vascular homeostasis --- atrial natriuretic peptide --- guanylyl cyclase/natriuretic peptide receptor-A --- gene-knockout --- gene-duplication --- hypertension --- congestive heart failure --- natriuretic peptides --- arterial hypertension --- pulmonary arterial hypertension --- heart failure --- stroke --- atrial fibrillation --- ARNi --- MANP

Research of Pathogenesis and Novel Therapeutics in Arthritis

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ISBN: 9783038970651 / 9783038970668 Year: Pages: 366 DOI: 10.3390/books978-3-03897-066-8 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General) --- Therapeutics
Added to DOAB on : 2019-06-26 08:44:06
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Arthritis has a high prevalence globally and includes over 100 different types, the most common of which are rheumatoid arthritis, osteoarthritis, psoriatic arthritis, and inflammatory arthritis. The exact etiology of arthritis remains unclear and no cure exists. Anti-inflammatory drugs are commonly used in the treatment of arthritis but are associated with significant side effects. Novel modes of therapy and additional prognostic biomarkers are urgently needed for arthritis patients. This book summarizes and discusses the global picture of the current understanding of arthritis.

Keywords

biosimilars --- Th9 lymphocytes --- rheumatoid arthritis --- infliximab --- rheumatoid arthritis --- bone erosion --- osteoblasts --- next-generation sequencing --- bioinformatics --- microRNA --- messenger RNA --- osteoarthritis --- cell signaling --- IL1? --- WNT --- antagonists --- computational modeling --- nitric oxide --- clodronate --- gene expression --- osteoarthritis --- progenitor cells --- SOX9 --- spondyloarthropathies --- inflammation --- mesenchymal stem cells --- visfatin --- IL-6 --- TNF-? --- osteoarthritis --- miR-199a-5p --- Epstein-Barr virus --- glycoprotein 42 --- rheumatoid arthritis --- shared epitope --- triptolide --- rheumatoid arthritis --- basic research --- clinical translation --- osteoarthritis (OA) --- articular cartilage --- molecular pathology --- therapeutics --- rheumatoid arthritis --- antibodies --- collagen --- glycosylation --- disease pathways --- therapy --- experimental arthritis --- TNF? --- etanercept --- infliximab --- adalimumab --- certolizumab pegol --- golimumab --- rheumatoid arthritis --- therapeutic antibody --- structure --- fraxinellone --- collagen-induced arthritis --- rheumatoid arthritis --- inflammatory arthritis --- osteoclastogenesis --- sclareol --- rheumatoid arthritis --- synovial cell --- collagen --- mice --- cytokines --- Th17 --- MAPK --- arthritis --- osteoarthritis --- rheumatoid arthritis --- small-molecule inhibitor --- chondrocytes --- tumor necrosis factor-alpha --- inflammation --- rheumatoid arthritis --- osteoarthritis --- angiogenesis --- cytokines --- chemokines --- early osteoarthritis --- articular cartilage --- proliferation --- fibroblast growth factor 2 --- mitogen activated protein kinase --- transforming growth factor ? --- SMA- and MAD-related protein --- interleukin --- nuclear factor kappa B --- miRNA --- adjuvant arthritis --- arthritis --- biomarkers --- celastrol --- inflammation --- microRNA --- miRNA --- rat --- rheumatoid arthritis --- Traditional Chinese medicine --- tripterine --- triterpenoid --- spinal fusion --- biological --- osteoblast --- osteoclast --- bisphosphonate --- parathyroid hormone --- bone morphogenetic protein --- receptor activator of nuclear factor ?B --- stem cell --- drug delivery system --- anticitrullinated peptide antibodies --- antirheumatic drug --- autoimmune --- disease-modifying --- immunology --- pathology --- rheumatoid factor --- rheumatoid arthritis --- osteoarthritis --- adipokines --- obesity --- rheumatoid arthritis --- osteoarthritis --- anti-arthritis --- biomarkers

Towards Mechanism-based Treatments for Fragile X Syndrome

Authors: ---
ISBN: 9783039215058 / 9783039215065 Year: Pages: 250 DOI: 10.3390/books978-3-03921-506-5 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Science (General) --- Biology
Added to DOAB on : 2019-12-09 11:49:15
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It has been more than 25 years since the identification of the FMR1 gene and the demonstration of the causative role of CGG-repeat expansion in the disease pathology of fragile X syndrome (FXS), but the underlying mechanisms involved in the expansion mutation and the resulting gene silencing still remain elusive. Our understanding of the pathways impacted by the loss of FMRP function has grown tremendously, and has opened new avenues for targeted treatments for FXS. However, the failure of recent clinical trials that were based on successful preclinical studies using the Fmr1 knockout mouse model has forced the scientific community to revisit clinical trial design and identify objective outcome measures. There has also been a renewed interest in restoring FMR1 gene expression as a possible treatment approach for FXS. This special issue of Brain Sciences highlights the progress that has been made towards understanding the disease mechanisms and how this has informed the development of treatment strategies that are being explored for FXS.

Keywords

fragile X syndrome --- clinical trials --- targeted treatments --- drug development --- fragile X syndrome --- clinical trials --- treatment development --- best practices --- fragile X syndrome --- newborn screening --- early identification --- fragile X syndrome --- X chromosome --- females --- FMR1 --- anxiety --- avoidance --- cognition --- behavior --- brain --- Fragile X --- FMRP --- Fxr2 --- Fmr1 --- fragile X syndrome --- executive function --- working memory --- set-shifting --- cognitive flexibility --- inhibitory control --- attention --- planning --- processing speed --- Fragile X syndrome 1 --- Fragile X-associated Tremor/Ataxia Syndrome 2 --- CRISPR 3 --- Trinucleotide Repeat 4 --- Gene editing --- fragile X syndrome --- FMR1 gene --- voice of the person --- voice of the patient --- characteristics that have the greatest impact --- developmental disorders --- fragile X syndrome --- language development --- automated vocal analysis --- adeno-associated virus --- autism spectrum disorders --- cerebral spinal fluid --- fragile X mental retardation protein --- neurodevelopmental disorders --- viral vector --- fragile X syndrome --- gene reactivation --- RNA:DNA hybrid --- FMRP --- histone methylation --- DNA methylation --- FMR1 --- PRC2 --- fragile X syndrome --- unstable repeat diseases --- epigenetic gene silencing --- DNA methylation --- repeat instability --- pluripotent stem cells --- CGG Repeat Expansion Disease --- DNA instability --- expansion --- contraction --- mismatch repair (MMR) --- base excision repair (BER) --- transcription coupled repair (TCR) --- double-strand break repair (DSBR) --- Non-homologous end-joining (NHEJ) --- mosaicism --- protein synthesis --- Fragile X Syndrome --- biomarker --- iPSC --- fibroblast --- lymphoblast --- fragile X syndrome --- molecular biomarkers --- FMR1 --- FMRP --- intellectual disability --- Fmr1 KO mouse --- ASD --- n/a

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