The SYSCID map: a graphical and computational resource of molecular mechanisms across rheumatoid arthritis, systemic lupus erythematosus and inflammatory bowel disease.

curation inflammatory bowel disease molecular mechanisms pathway biology rheumatoid arthritis systemic lupus erythematosus systems biology

Journal

Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960

Informations de publication

Date de publication:
2023
Historique:
received: 12 07 2023
accepted: 16 10 2023
medline: 1 12 2023
pubmed: 29 11 2023
entrez: 29 11 2023
Statut: epublish

Résumé

Chronic inflammatory diseases (CIDs), including inflammatory bowel disease (IBD), rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) are thought to emerge from an impaired complex network of inter- and intracellular biochemical interactions among several proteins and small chemical compounds under strong influence of genetic and environmental factors. CIDs are characterised by shared and disease-specific processes, which is reflected by partially overlapping genetic risk maps and pathogenic cells (e.g., T cells). Their pathogenesis involves a plethora of intracellular pathways. The translation of the research findings on CIDs molecular mechanisms into effective treatments is challenging and may explain the low remission rates despite modern targeted therapies. Modelling CID-related causal interactions as networks allows us to tackle the complexity at a systems level and improve our understanding of the interplay of key pathways. Here we report the construction, description, and initial applications of the SYSCID map (https://syscid.elixir-luxembourg.org/), a mechanistic causal interaction network covering the molecular crosstalk between IBD, RA and SLE. We demonstrate that the map serves as an interactive, graphical review of IBD, RA and SLE molecular mechanisms, and helps to understand the complexity of omics data. Examples of such application are illustrated using transcriptome data from time-series gene expression profiles following anti-TNF treatment and data from genome-wide associations studies that enable us to suggest potential effects to altered pathways and propose possible mechanistic biomarkers of treatment response.

Identifiants

pubmed: 38022524
doi: 10.3389/fimmu.2023.1257321
pmc: PMC10646502
doi:

Substances chimiques

Tumor Necrosis Factor Inhibitors 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1257321

Informations de copyright

Copyright © 2023 Acencio, Ostaszewski, Mazein, Rosenstiel, Aden, Mishra, Andersen, Sidiropoulos, Banos, Filia, Rahmouni, Finckh, Gu, Schneider and Satagopam.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision.

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Auteurs

Marcio Luis Acencio (ML)

Luxembourg Centre for Systems Biomedicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg.

Marek Ostaszewski (M)

Luxembourg Centre for Systems Biomedicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg.
ELIXIR Luxembourg, Esch-sur-Alzette, Luxembourg.

Alexander Mazein (A)

Luxembourg Centre for Systems Biomedicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg.

Philip Rosenstiel (P)

Institute of Clinical Molecular Biology, Christian-Albrechts-University Kiel and University Medical Center Schleswig-Holstein, Kiel, Germany.

Konrad Aden (K)

Institute of Clinical Molecular Biology, Christian-Albrechts-University Kiel and University Medical Center Schleswig-Holstein, Kiel, Germany.
Department of Internal Medicine I, University Medical Center Schleswig-Holstein, Kiel, Germany.

Neha Mishra (N)

Institute of Clinical Molecular Biology, Christian-Albrechts-University Kiel and University Medical Center Schleswig-Holstein, Kiel, Germany.

Vibeke Andersen (V)

Diagnostics and Clinical Research Unit, Institute of Regional Health Research, University Hospital of Southern Denmark, Aabenraa, Denmark.
Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark.

Prodromos Sidiropoulos (P)

Rheumatology and Clinical Immunology, Medical School, University of Crete, Heraklion, Greece.
Laboratory of Rheumatology, Autoimmunity and Inflammation, Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology (IMBB-FORTH), Heraklion, Greece.

Aggelos Banos (A)

Autoimmunity and Inflammation Laboratory, Biomedical Research Foundation of the Academy of Athens, Athens and Laboratory of Molecular Hematology, Democritus University of Thrace, University Hospital of Alexandroupolis, Alexandroupolis, Greece.

Anastasia Filia (A)

Autoimmunity and Inflammation Laboratory, Biomedical Research Foundation of the Academy of Athens, Athens and Laboratory of Molecular Hematology, Democritus University of Thrace, University Hospital of Alexandroupolis, Alexandroupolis, Greece.

Souad Rahmouni (S)

Unit of Animal Genomics, GIGA-Institute, University of Liège, Liège, Belgium.

Axel Finckh (A)

Rheumatology Division, Geneva University Hospital (HUG), Geneva, Switzerland.
Geneva Center for Inflammation Research (GCIR), University of Geneva (UNIGE), Geneva, Switzerland.

Wei Gu (W)

Luxembourg Centre for Systems Biomedicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg.
ELIXIR Luxembourg, Esch-sur-Alzette, Luxembourg.

Reinhard Schneider (R)

Luxembourg Centre for Systems Biomedicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg.
ELIXIR Luxembourg, Esch-sur-Alzette, Luxembourg.

Venkata Satagopam (V)

Luxembourg Centre for Systems Biomedicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg.
ELIXIR Luxembourg, Esch-sur-Alzette, Luxembourg.

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