TL;DR
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...
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...
A review of the sources of DAMPs and their recognition mechanisms in the OA microenvironment, with particular attention to their potential links with trained immunity in monocyte–macrophage populations, and summarizes therapeutic opportunities potentially relevant to the proposed links between DAMP signaling and traine...
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...
This chapter outlines the cellular and molecular mechanisms governing efferocytosis and SPM signalling and how these processes become disrupted during plaque progression, contributing to persistent inflammation and defective clearance of dying cells in atherosclerotic plaques.
We use cookies to run the site and, with your consent, for analytics and to show ads. See our Cookie Policy.
