scholarly journals Cartilage and Bone Destruction in Arthritis: Pathogenesis and Treatment Strategy: A Literature Review

Cells ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 818 ◽  
Author(s):  
Tateiwa ◽  
Yoshikawa ◽  
Kaito
Keyword(s):  
Rheumatoid Arthritis ◽  
Signaling Pathways ◽  
Immune Cells ◽  
Intracellular Signaling ◽  
Bone Destruction ◽  
Therapeutic Strategies ◽  
Intracellular Signaling Pathways ◽  
Extracellular Signaling ◽  
Intracellular Signals ◽  
Novel Therapeutic

Arthritis is inflammation of the joints accompanied by osteochondral destruction. It can take many forms, including osteoarthritis, rheumatoid arthritis, and psoriatic arthritis. These diseases share one commonality—osteochondral destruction based on inflammation. The background includes a close interaction between osseous tissues and immune cells through various inflammatory cytokines. However, the tissues and cytokines that play major roles are different in each disease, and as a result, the mechanism of osteochondral destruction also differs. In recent years, there have been many findings regarding not only extracellular signaling pathways but also intracellular signaling pathways. In particular, we anticipate that the intracellular signals of osteoclasts, which play a central role in bone destruction, will become novel therapeutic targets. In this review, we have summarized the pathology of arthritis and the latest findings on the mechanism of osteochondral destruction, as well as present and future therapeutic strategies for these targets.

scholarly journals Collapsing the list of myocardial infarction-related differential expressed genes into a diagnostic signature

2020 ◽  
Author(s):  
German Osmak ◽  
Natalia Baulina ◽  
Philipp Koshkin ◽  
Olga Favorova
Keyword(s):  
Myocardial Infarction ◽  
Signaling Pathways ◽  
Immune Cells ◽  
Intracellular Signaling ◽  
Mononuclear Cells ◽  
Learning Algorithm ◽  
Classification Model ◽  
Central Component ◽  
Intracellular Signaling Pathways ◽  
Differential Expressed Genes

AbstractMyocardial infarction (MI) is one of the most severe manifestations of coronary artery disease (CAD) and the leading cause of death from non-infectious diseases worldwide. It is known that the central component of CAD pathogenesis is a chronic vascular inflammation. However, the mechanisms underlying the changes that occur in T, B and NK lymphocytes, monocytes and other immune cells during CAD and MI are still poorly understood. One of those pathogenic mechanisms might be the dysregulation of intracellular signaling pathways in the immune cells.In the present study we performed a transcriptome profiling in peripheral blood mononuclear cells of MI patients and controls. The machine learning algorithm was then used to search for MI-associated signatures, that could reflect the dysregulation of intracellular signaling pathways.The genes ADAP2, KLRC1, MIR21, PDGFD and CD14 were identified as the most important signatures for the classification model with L1-norm penalty function. The classifier output quality was equal to 0.911 by Receiver Operating Characteristic metric on test data. These results were validated on two independent open GEO datasets. Identified MI-associated signatures can be further assisted in MI diagnosis and/or prognosis.Thus, our study presents a pipeline for collapsing the list of differential expressed genes, identified by high-throughput techniques, in order to define disease-associated diagnostic signatures.

scholarly journals Sex-Based Differences in the Cytokine Production and Intracellular Signaling Pathways in Patients With Rheumatoid Arthritis

2020 ◽  
Vol 35 (4) ◽  
pp. 545-557
Author(s):  
Uday P. PRATAP ◽  
Lalgi HIMA ◽  
Thangamani KANNAN ◽  
Chadrasekaran THYAGARAJAN ◽  
Hannah P. PRIYANKA ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Cytokine Production ◽  
Intracellular Signaling Pathways

Targeting intracellular signaling pathways to treat rheumatoid arthritis: Pandora's box?

2010 ◽  
Vol 77 (2) ◽  
pp. 96-98 ◽  
Author(s):  
Daniel Wendling ◽  
Clément Prati ◽  
Éric Toussirot ◽  
Georges Herbein
Keyword(s):  
Rheumatoid Arthritis ◽  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Intracellular Signaling Pathways

scholarly journals What Do We Have to Know about PD-L1 Expression in Prostate Cancer? A Systematic Literature Review. Part 3: PD-L1, Intracellular Signaling Pathways and Tumor Microenvironment

2021 ◽  
Vol 22 (22) ◽  
pp. 12330
Author(s):  
Andrea Palicelli ◽  
Stefania Croci ◽  
Alessandra Bisagni ◽  
Eleonora Zanetti ◽  
Dario De Biase ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Microenvironment ◽  
Literature Review ◽  
Signaling Pathways ◽  
Systematic Literature Review ◽  
Immune Cells ◽  
Intracellular Signaling ◽  
Immune Escape ◽  
Tumor Immune Escape ◽  
Intracellular Signaling Pathways

The tumor microenvironment (TME) includes immune (T, B, NK, dendritic), stromal, mesenchymal, endothelial, adipocytic cells, extracellular matrix, and cytokines/chemokines/soluble factors regulating various intracellular signaling pathways (ISP) in tumor cells. TME influences the survival/progression of prostate cancer (PC), enabling tumor cell immune-evasion also through the activation of the PD-1/PD-L1 axis. We have performed a systematic literature review according to the PRISMA guidelines, to investigate how the PD-1/PD-L1 pathway is influenced by TME and ISPs. Tumor immune-escape mechanisms include suppression/exhaustion of tumor infiltrating cytotoxic T lymphocytes, inhibition of tumor suppressive NK cells, increase in immune-suppressive immune cells (regulatory T, M2 macrophagic, myeloid-derived suppressor, dendritic, stromal, and adipocytic cells). IFN-γ (the most investigated factor), TGF-β, TNF-α, IL-6, IL-17, IL-15, IL-27, complement factor C5a, and other soluble molecules secreted by TME components (and sometimes increased in patients’ serum), as well as and hypoxia, influenced the regulation of PD-L1. Experimental studies using human and mouse PC cell lines (derived from either androgen-sensitive or androgen-resistant tumors) revealed that the intracellular ERK/MEK, Akt-mTOR, NF-kB, WNT and JAK/STAT pathways were involved in PD-L1 upregulation in PC. Blocking the PD-1/PD-L1 signaling by using immunotherapy drugs can prevent tumor immune-escape, increasing the anti-tumor activity of immune cells.

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