The immunosuppressive activity of artemisinin-type drugs towards inflammatory and autoimmune diseases

Publikationstyp:
Zeitschriftenaufsatz
Metadaten:
Autoren
Autoren-URL
https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=fis-test-1&SrcAuth=WosAPI&KeyUT=WOS:000675086500001&DestLinkType=FullRecord&DestApp=WOS_CPL
DOI
10.1002/med.21842
eISSN
1098-1128
Externe Identifier
  • Clarivate Analytics Document Solution ID: WD9KI
  • PubMed Identifier: 34288018
ISSN
0198-6325
Ausgabe der Veröffentlichung
6
Zeitschrift
MEDICINAL RESEARCH REVIEWS
Schlüsselwörter
  • arthritis
  • asthma
  • dermatitis
  • immunity
  • inflammatory bowel disease
  • natural product
  • neuroinflammation
  • traditional Chinese medicine
Paginierung
3023 - 3061
Datum der Veröffentlichung
2021
Status
Published
Titel
The immunosuppressive activity of artemisinin-type drugs towards inflammatory and autoimmune diseases
Sub types
  • Review
Ausgabe der Zeitschrift
41

Datenquelle: Web of Science (Lite)

Andere Metadatenquellen:
Abstract
<jats:title>Abstract</jats:title><jats:p>The sesquiterpene lactone artemisinin from <jats:italic>Artemisia annua</jats:italic> L. is well established for malaria therapy, but its bioactivity spectrum is much broader. In this review, we give a comprehensive and timely overview of the literature regarding the immunosuppressive activity of artemisinin‐type compounds toward inflammatory and autoimmune diseases. Numerous receptor‐coupled signaling pathways are inhibited by artemisinins, including the receptors for interleukin‐1 (IL‐1), tumor necrosis factor‐α (TNF‐α), β3‐integrin, or RANKL, toll‐like receptors and growth factor receptors. Among the receptor‐coupled signal transducers are extracellular signal‐regulated protein kinase (ERK), c‐Jun N‐terminal kinase (JNK), phosphatidylinositol‐4,5‐bisphosphate 3‐kinase (PI3K), AKT serine/threonine kinase (AKT), mitogen‐activated protein kinase (MAPK)/extracellular signal regulated kinase (ERK) kinase (MEK), phospholipase C γ1 (PLCγ), and others. All these receptors and signal transduction molecules are known to contribute to the inhibition of the transcription factor nuclear factor κ B (NF‐κB). Artemisinins may inhibit NF‐κB by silencing these upstream pathways and/or by direct binding to NF‐κB. Numerous NF‐κB‐regulated downstream genes are downregulated by artemisinin and its derivatives, for example, cytokines, chemokines, and immune receptors, which regulate immune cell differentiation, apoptosis genes, proliferation‐regulating genes, signal transducers, and genes involved in antioxidant stress response. In addition to the prominent role of NF‐κB, other transcription factors are also inhibited by artemisinins (mammalian target of rapamycin [mTOR], activating protein 1 [AP1]/FBJ murine osteosarcoma viral oncogene homologue [FOS]/JUN oncogenic transcription factor [JUN]), hypoxia‐induced factor 1α (HIF‐1α), nuclear factor of activated T cells c1 (NF‐ATC1), Signal transducers and activators of transcription (STAT), NF E2‐related factor‐2 (NRF‐2), retinoic‐acid‐receptor‐related orphan nuclear receptor γ (ROR‐γt), and forkhead box P‐3 (FOXP‐3). Many in vivo experiments in disease‐relevant animal models demonstrate therapeutic efficacy of artemisinin‐type drugs against rheumatic diseases (rheumatoid arthritis, osteoarthritis, lupus erythematosus, arthrosis, and gout), lung diseases (asthma, acute lung injury, and pulmonary fibrosis), neurological diseases (autoimmune encephalitis, Alzheimer's disease, and myasthenia gravis), skin diseases (dermatitis, rosacea, and psoriasis), inflammatory bowel disease, and other inflammatory and autoimmune diseases. Randomized clinical trials should be conducted in the future to translate the plethora of preclinical results into clinical practice.</jats:p>
Autoren
DOI
10.1002/med.21842
eISSN
1098-1128
ISSN
0198-6325
Ausgabe der Veröffentlichung
6
Zeitschrift
Medicinal Research Reviews
Sprache
en
Online publication date
2021
Paginierung
3023 - 3061
Datum der Veröffentlichung
2021
Status
Published
Herausgeber
Wiley
Herausgeber URL
http://dx.doi.org/10.1002/med.21842
Datum der Datenerfassung
2023
Titel
The immunosuppressive activity of artemisinin‐type drugs towards inflammatory and autoimmune diseases
Ausgabe der Zeitschrift
41

Datenquelle: Crossref

Abstract
The sesquiterpene lactone artemisinin from Artemisia annua L. is well established for malaria therapy, but its bioactivity spectrum is much broader. In this review, we give a comprehensive and timely overview of the literature regarding the immunosuppressive activity of artemisinin-type compounds toward inflammatory and autoimmune diseases. Numerous receptor-coupled signaling pathways are inhibited by artemisinins, including the receptors for interleukin-1 (IL-1), tumor necrosis factor-α (TNF-α), β3-integrin, or RANKL, toll-like receptors and growth factor receptors. Among the receptor-coupled signal transducers are extracellular signal-regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK), phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K), AKT serine/threonine kinase (AKT), mitogen-activated protein kinase (MAPK)/extracellular signal regulated kinase (ERK) kinase (MEK), phospholipase C γ1 (PLCγ), and others. All these receptors and signal transduction molecules are known to contribute to the inhibition of the transcription factor nuclear factor κ B (NF-κB). Artemisinins may inhibit NF-κB by silencing these upstream pathways and/or by direct binding to NF-κB. Numerous NF-κB-regulated downstream genes are downregulated by artemisinin and its derivatives, for example, cytokines, chemokines, and immune receptors, which regulate immune cell differentiation, apoptosis genes, proliferation-regulating genes, signal transducers, and genes involved in antioxidant stress response. In addition to the prominent role of NF-κB, other transcription factors are also inhibited by artemisinins (mammalian target of rapamycin [mTOR], activating protein 1 [AP1]/FBJ murine osteosarcoma viral oncogene homologue [FOS]/JUN oncogenic transcription factor [JUN]), hypoxia-induced factor 1α (HIF-1α), nuclear factor of activated T cells c1 (NF-ATC1), Signal transducers and activators of transcription (STAT), NF E2-related factor-2 (NRF-2), retinoic-acid-receptor-related orphan nuclear receptor γ (ROR-γt), and forkhead box P-3 (FOXP-3). Many in vivo experiments in disease-relevant animal models demonstrate therapeutic efficacy of artemisinin-type drugs against rheumatic diseases (rheumatoid arthritis, osteoarthritis, lupus erythematosus, arthrosis, and gout), lung diseases (asthma, acute lung injury, and pulmonary fibrosis), neurological diseases (autoimmune encephalitis, Alzheimer's disease, and myasthenia gravis), skin diseases (dermatitis, rosacea, and psoriasis), inflammatory bowel disease, and other inflammatory and autoimmune diseases. Randomized clinical trials should be conducted in the future to translate the plethora of preclinical results into clinical practice.
Addresses
  • Department of Pharmaceutical Biology, Institute of Pharmaceutical and Biomedical Sciences, Johannes Gutenberg University, Mainz, Germany.
Autoren
DOI
10.1002/med.21842
eISSN
1098-1128
Externe Identifier
  • PubMed Identifier: 34288018
Open access
false
ISSN
0198-6325
Ausgabe der Veröffentlichung
6
Zeitschrift
Medicinal research reviews
Schlüsselwörter
  • Humans
  • Autoimmune Diseases
  • Artemisinins
  • NF-kappa B
  • Immunosuppressive Agents
  • Signal Transduction
Sprache
eng
Medium
Print-Electronic
Online publication date
2021
Paginierung
3023 - 3061
Datum der Veröffentlichung
2021
Status
Published
Publisher licence
CC BY
Datum der Datenerfassung
2021
Titel
The immunosuppressive activity of artemisinin-type drugs towards inflammatory and autoimmune diseases.
Sub types
  • Research Support, Non-U.S. Gov't
  • Review
  • Journal Article
Ausgabe der Zeitschrift
41

Datenquelle: Europe PubMed Central

Abstract
The sesquiterpene lactone artemisinin from Artemisia annua L. is well established for malaria therapy, but its bioactivity spectrum is much broader. In this review, we give a comprehensive and timely overview of the literature regarding the immunosuppressive activity of artemisinin-type compounds toward inflammatory and autoimmune diseases. Numerous receptor-coupled signaling pathways are inhibited by artemisinins, including the receptors for interleukin-1 (IL-1), tumor necrosis factor-α (TNF-α), β3-integrin, or RANKL, toll-like receptors and growth factor receptors. Among the receptor-coupled signal transducers are extracellular signal-regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK), phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K), AKT serine/threonine kinase (AKT), mitogen-activated protein kinase (MAPK)/extracellular signal regulated kinase (ERK) kinase (MEK), phospholipase C γ1 (PLCγ), and others. All these receptors and signal transduction molecules are known to contribute to the inhibition of the transcription factor nuclear factor κ B (NF-κB). Artemisinins may inhibit NF-κB by silencing these upstream pathways and/or by direct binding to NF-κB. Numerous NF-κB-regulated downstream genes are downregulated by artemisinin and its derivatives, for example, cytokines, chemokines, and immune receptors, which regulate immune cell differentiation, apoptosis genes, proliferation-regulating genes, signal transducers, and genes involved in antioxidant stress response. In addition to the prominent role of NF-κB, other transcription factors are also inhibited by artemisinins (mammalian target of rapamycin [mTOR], activating protein 1 [AP1]/FBJ murine osteosarcoma viral oncogene homologue [FOS]/JUN oncogenic transcription factor [JUN]), hypoxia-induced factor 1α (HIF-1α), nuclear factor of activated T cells c1 (NF-ATC1), Signal transducers and activators of transcription (STAT), NF E2-related factor-2 (NRF-2), retinoic-acid-receptor-related orphan nuclear receptor γ (ROR-γt), and forkhead box P-3 (FOXP-3). Many in vivo experiments in disease-relevant animal models demonstrate therapeutic efficacy of artemisinin-type drugs against rheumatic diseases (rheumatoid arthritis, osteoarthritis, lupus erythematosus, arthrosis, and gout), lung diseases (asthma, acute lung injury, and pulmonary fibrosis), neurological diseases (autoimmune encephalitis, Alzheimer's disease, and myasthenia gravis), skin diseases (dermatitis, rosacea, and psoriasis), inflammatory bowel disease, and other inflammatory and autoimmune diseases. Randomized clinical trials should be conducted in the future to translate the plethora of preclinical results into clinical practice.
Date of acceptance
2021
Autoren
Autoren-URL
https://www.ncbi.nlm.nih.gov/pubmed/34288018
DOI
10.1002/med.21842
eISSN
1098-1128
Ausgabe der Veröffentlichung
6
Zeitschrift
Med Res Rev
Schlüsselwörter
  • arthritis
  • asthma
  • dermatitis
  • immunity
  • inflammatory bowel disease
  • natural product
  • neuroinflammation
  • traditional Chinese medicine
  • Artemisinins
  • Autoimmune Diseases
  • Humans
  • Immunosuppressive Agents
  • NF-kappa B
  • Signal Transduction
Sprache
eng
Country
United States
Paginierung
3023 - 3061
Datum der Veröffentlichung
2021
Status
Published
Datum, an dem der Datensatz öffentlich gemacht wurde
2022
Titel
The immunosuppressive activity of artemisinin-type drugs towards inflammatory and autoimmune diseases.
Sub types
  • Journal Article
  • Research Support, Non-U.S. Gov't
  • Review
Ausgabe der Zeitschrift
41

Datenquelle: PubMed

Author's licence
CC-BY
Autoren
Hosting institution
Universitätsbibliothek Mainz
Sammlungen
  • JGU-Publikationen
Resource version
Published version
DOI
10.1002/med.21842
File(s) embargoed
false
Open access
true
ISSN
1098-1128
Ausgabe der Veröffentlichung
6
Zeitschrift
Medicinal research reviews
Schlüsselwörter
  • 570 Biowissenschaften
  • 570 Life sciences
Sprache
eng
Open access status
Open Access
Paginierung
3023 - 3061
Datum der Veröffentlichung
2021
Public URL
https://openscience.ub.uni-mainz.de/handle/20.500.12030/8083
Herausgeber
Wiley Interscience
Datum der Datenerfassung
2022
Datum, an dem der Datensatz öffentlich gemacht wurde
2022
Zugang
Public
Titel
The immunosuppressive activity of artemisinin-type drugs towards inflammatory and autoimmune diseases
Ausgabe der Zeitschrift
41

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