An Update on the Emerging Role of Wnt/β-catenin, SYK, PI3K/AKT, and GM-CSF Signaling Pathways in Rheumatoid Arthritis
Copyright© Bentham Science Publishers; For any queries, please email at epubbenthamscience.net..
Rheumatoid arthritis is an untreatable autoimmune disorder. The disease is accompanied by joint impairment and anomalies, which negatively affect the patient's quality of life and contribute to a decline in manpower. To diagnose and treat rheumatoid arthritis, it is crucial to understand the abnormal signaling pathways that contribute to the disease. This understanding will help develop new rheumatoid arthritis-related intervention targets. Over the last few decades, researchers have given more attention to rheumatoid arthritis. The current review seeks to provide a detailed summary of rheumatoid arthritis, highlighting the basic description of the disease, past occurrences, the study of epidemiology, risk elements, and the process of disease progression, as well as the key scientific development of the disease condition and multiple signaling pathways and enumerating the most current advancements in discovering new rheumatoid arthritis signaling pathways and rheumatoid arthritis inhibitors. This review emphasizes the anti-rheumatoid effects of these inhibitors [for the Wnt/β-catenin, Phosphoinositide 3-Kinases (PI3K/AKT), Spleen Tyrosine Kinase (SYK), and Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF) signaling pathways], illustrating their mechanism of action through a literature search, current therapies, and novel drugs under pre-clinical and clinical trials.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2023 |
|---|---|
| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:24 |
|---|---|
| Enthalten in: |
Current drug targets - 24(2023), 17 vom: 11., Seite 1298-1316 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Prajapati, Pradyuman [VerfasserIn] |
|---|
| Links: |
|---|
| Anmerkungen: |
Date Completed 08.01.2024 Date Revised 08.01.2024 published: Print Citation Status MEDLINE |
|---|
| doi: |
10.2174/0113894501276093231206064243 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM365746568 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM365746568 | ||
| 003 | DE-627 | ||
| 005 | 20240114232054.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231226s2023 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.2174/0113894501276093231206064243 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1252.xml |
| 035 | |a (DE-627)NLM365746568 | ||
| 035 | |a (NLM)38083893 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Prajapati, Pradyuman |e verfasserin |4 aut | |
| 245 | 1 | 3 | |a An Update on the Emerging Role of Wnt/β-catenin, SYK, PI3K/AKT, and GM-CSF Signaling Pathways in Rheumatoid Arthritis |
| 264 | 1 | |c 2023 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 08.01.2024 | ||
| 500 | |a Date Revised 08.01.2024 | ||
| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright© Bentham Science Publishers; For any queries, please email at epubbenthamscience.net. | ||
| 520 | |a Rheumatoid arthritis is an untreatable autoimmune disorder. The disease is accompanied by joint impairment and anomalies, which negatively affect the patient's quality of life and contribute to a decline in manpower. To diagnose and treat rheumatoid arthritis, it is crucial to understand the abnormal signaling pathways that contribute to the disease. This understanding will help develop new rheumatoid arthritis-related intervention targets. Over the last few decades, researchers have given more attention to rheumatoid arthritis. The current review seeks to provide a detailed summary of rheumatoid arthritis, highlighting the basic description of the disease, past occurrences, the study of epidemiology, risk elements, and the process of disease progression, as well as the key scientific development of the disease condition and multiple signaling pathways and enumerating the most current advancements in discovering new rheumatoid arthritis signaling pathways and rheumatoid arthritis inhibitors. This review emphasizes the anti-rheumatoid effects of these inhibitors [for the Wnt/β-catenin, Phosphoinositide 3-Kinases (PI3K/AKT), Spleen Tyrosine Kinase (SYK), and Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF) signaling pathways], illustrating their mechanism of action through a literature search, current therapies, and novel drugs under pre-clinical and clinical trials | ||
| 650 | 4 | |a Review | |
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Rheumatoid arthritis | |
| 650 | 4 | |a Wnt/β-catenin | |
| 650 | 4 | |a autoimmune disorder | |
| 650 | 4 | |a granulocyte- macrophage colony stimulating factor (GM-CSF) | |
| 650 | 4 | |a inflammation. | |
| 650 | 4 | |a novel targets | |
| 650 | 4 | |a phosphoinositide 3- kinases (PI3K/AKT) | |
| 650 | 4 | |a spleen tyrosine kinase (SYK) | |
| 650 | 7 | |a Granulocyte-Macrophage Colony-Stimulating Factor |2 NLM | |
| 650 | 7 | |a 83869-56-1 |2 NLM | |
| 650 | 7 | |a Phosphatidylinositol 3-Kinases |2 NLM | |
| 650 | 7 | |a EC 2.7.1.- |2 NLM | |
| 650 | 7 | |a Proto-Oncogene Proteins c-akt |2 NLM | |
| 650 | 7 | |a EC 2.7.11.1 |2 NLM | |
| 650 | 7 | |a beta Catenin |2 NLM | |
| 650 | 7 | |a SYK protein, human |2 NLM | |
| 650 | 7 | |a EC 2.7.10.2 |2 NLM | |
| 650 | 7 | |a Syk Kinase |2 NLM | |
| 650 | 7 | |a EC 2.7.10.2 |2 NLM | |
| 700 | 1 | |a Doshi, Gaurav |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Current drug targets |d 2000 |g 24(2023), 17 vom: 11., Seite 1298-1316 |w (DE-627)NLM113669291 |x 1873-5592 |7 nnns |
| 773 | 1 | 8 | |g volume:24 |g year:2023 |g number:17 |g day:11 |g pages:1298-1316 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.2174/0113894501276093231206064243 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 24 |j 2023 |e 17 |b 11 |h 1298-1316 | ||