<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>18(12)</volume><submitter>Aghakhani S</submitter><funding>Ecoles doctorales, Université Paris-Saclay</funding><funding>Genopole</funding><funding>Institut national de recherche en informatique et en automatique</funding><pubmed_abstract>Rheumatoid Arthritis (RA) is an autoimmune disease characterized by a highly invasive pannus formation consisting mainly of Synovial Fibroblasts (RASFs). This pannus leads to cartilage, bone, and soft tissue destruction in the affected joint. RASFs' activation is associated with metabolic alterations resulting from dysregulation of extracellular signals' transduction and gene regulation. Deciphering the intricate mechanisms at the origin of this metabolic reprogramming may provide sign insight into RASFs' involvement in RA's pathogenesis and offer new therapeutic strategies. Qualitative and quantitative dynamic modeling can address some of these features, but hybrid models represent a real asset in their ability to span multiple layers of biological machinery. This work presents the first </pubmed_abstract><journal>PLoS computational biology</journal><pagination>e1010408</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9779668</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Metabolic reprogramming in Rheumatoid Arthritis Synovial Fibroblasts: A hybrid modeling approach.</pubmed_title><pmcid>PMC9779668</pmcid><pubmed_authors>Niarakis A</pubmed_authors><pubmed_authors>Aghakhani S</pubmed_authors><pubmed_authors>Soliman S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Metabolic reprogramming in Rheumatoid Arthritis Synovial Fibroblasts: A hybrid modeling approach.</name><description>Rheumatoid Arthritis (RA) is an autoimmune disease characterized by a highly invasive pannus formation consisting mainly of Synovial Fibroblasts (RASFs). This pannus leads to cartilage, bone, and soft tissue destruction in the affected joint. RASFs' activation is associated with metabolic alterations resulting from dysregulation of extracellular signals' transduction and gene regulation. Deciphering the intricate mechanisms at the origin of this metabolic reprogramming may provide sign insight into RASFs' involvement in RA's pathogenesis and offer new therapeutic strategies. Qualitative and quantitative dynamic modeling can address some of these features, but hybrid models represent a real asset in their ability to span multiple layers of biological machinery. This work presents the first </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2025-04-18T17:14:49.303Z</modification><creation>2025-04-07T04:48:02.571Z</creation></dates><accession>S-EPMC9779668</accession><cross_references><pubmed>36508473</pubmed><doi>10.1371/journal.pcbi.1010408</doi></cross_references></HashMap>