In this Review, the authors provide insights into the role of hypoxia in the pathogenesis of RA, its role in the wider integrated signalling network that drives inflammation and how hypoxia can be targeted therapeutically to treat RA are highlighted.
Osteoarthritis (OA) is a whole-joint disease involving cartilage, synovium, subchondral bone, and neurovascular structures. Synovitis, damage-associated molecular patterns, and interactions between macrophages and fibroblast-like synoviocytes have been widely studied. However, a tissue-level explanation is still lackin...
Kang-Yi Hu, Yong-Jia Song, Jia-Xing Pan et al.· Frontiers in Immunology· 0 citations
Osteoarthritis (OA) has conventionally been considered a degenerative mechanical condition; but an increasing number of studies support an alternative perception of this disease as one characterized by impaired immune homeostasis in the joint environment. The purpose of this review is to analyze the mechanisms of how t...
This review examines how metabolic pathways, particularly the balance between glycolysis and oxidative phosphorylation, govern macrophage behavior through epigenetic mechanisms, thereby coupling cellular metabolism to inflammatory and regenerative gene expression and how these interconnected pathways are disrupted in c...
Sarah Tiufekchiev-Grieco, James S. Novak, J. Jaiswal· Frontiers in Immunology· 1 citation
Osteoarthritis (OA) is now widely discussed as a whole-joint immunometabolic disease involving cartilage, synovium, and subchondral bone, rather than as cartilage degeneration driven only by mechanical stress. Tissue injury, cell death, mitochondrial dysfunction, and extracellular matrix degradation can lead to the per...
Abstract Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent synovitis and progressive structural joint damage. Its pathology involves immune-cell infiltration, pannus formation, cartilage degradation, and bone destruction. Although autoantibodies, inflammatory cytokines, and aberrant...
Ting-Ting Li, Guang-Huan Li, Yu-Yao Yang et al.· Journal of Inflammation Rese...· 0 citations