ReviewNature reviews. Rheumatology2022
Cellular metabolic adaptations in rheumatoid arthritis and their therapeutic implications.
Review in Nature reviews. Rheumatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- Mechanistic role of quercetin as inhibitor for adenosine deaminase enzyme in rheumatoid arthritis: systematic review.Cellular & molecular biology letters · 2024Pooled it
- Hypoxia as an amplifier of synovial inflammation in rheumatoid arthritis.Nature reviews. Rheumatology · 2026Review
- Metabolic exhaustion and immune ageing in rheumatoid arthritis.Nature reviews. Rheumatology · 2026Review
- Investigating the Link Between Specific Signaling Molecules (CCL5, CCR5, CXCR4, BMPR2) and Cardiac Health Indicators in Rheumatoid Arthritis Individuals: A Cross-Sectional Study.Health science reports · 2026Article
- Article
- Metabolic reprogramming in polyol pathway contributes to anti-inflammatory effect of glucosamine salts on synovial fibroblasts.npj metabolic health and disease · 2026Article
- Point-of-care Diagnostic Framework for Fibromyalgia Using Integrated Vibrational Spectroscopy and Metabolomics.Research square · 2026Article
- Lactate programs CRIP1 protein lactylation to drive synovial proliferation in rheumatoid arthritis.JCI insight · 2026Article
- Metabolic and neuroimmune control of rheumatoid arthritis: therapeutic implications of FXR and α7-nAChR axes.Inflammopharmacology · 2026Review
- pH-Responsive Cinnamaldehyde-Arginine Nanoprodrug for Targeted Rheumatoid Arthritis Therapy via Antioxidant Activity and Macrophage Reprogramming.Antioxidants (Basel, Switzerland) · 2026Article
- Tofacitinib repairs inflammation and mitochondrial dysregulation in GM-CSF-reprogrammed RA macrophages.Cellular & molecular immunology · 2026Article
- Ginsenoside Re regulates PFKFB3-mediated glycolysis to inhibit endothelial cell migration to ameliorate atherosclerosis.Journal of ginseng research · 2026Article
- Hydrogel microspheres loaded with sinomenine and Drynaria rhizome enhance the treatment of rheumatoid arthritis via immune regulation and promoting bone repair.Journal of nanobiotechnology · 2026Article
- Identification of Immune-Related Lactylation Genes in Rheumatoid Arthritis With Atherosclerosis: A Comprehensive Analysis Using Bulk and Single-Cell RNA Sequencing Data.Mediators of inflammation · 2026Article
- From Systemic Autoimmunity to the Local Immune Niche of the Synovium: New Insights into the Development of Rheumatoid Arthritis.Journal of inflammation research · 2026Review
- Mechanism of HIF-1α-mediated angiogenesis in rheumatoid arthritis and progress of natural medicine interventions.Frontiers in pharmacology · 2026Review
- Immunometabolism in rheumatoid arthritis: mechanisms, biomarkers, and the path to precision medicine.Frontiers in immunology · 2026Review
- Succinate-mediated metabolic alterations and signaling in RA: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Bioengineered photosynthetic nanothylakoids reshape the inflammatory microenvironment for rheumatoid arthritis therapy.Nature nanotechnology · 2026Article
- The dual role of metabolic reprogramming in macrophage polarization in rheumatoid arthritis and coronary heart disease and the intervention strategy of traditional Chinese medicine.Frontiers in cardiovascular medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of endothelium and immune cells is fundamental to the initiation of autoimmune diseases such as rheumatoid arthritis (RA), and it results in trans-endothelial cell migration and synovial fibroblast proliferation, leading to joint destruction. In RA, the synovial microvasculature is highly dysregulated, resulting in inefficient oxygen perfusion to the synovium, which, along with the high metabolic demands of activated immune and stromal cells, leads to a profoundly hypoxic microenvironment. In inflamed joints, infiltrating immune cells and synovial resident cells have great requirements for energy and nutrients, and they adapt their metabolic profiles to generate sufficient energy to support their highly activated inflammatory states. This shift in metabolic capacity of synovial cells enables them to produce the essential building blocks to support their proliferation, activation and invasiveness. Furthermore, it results in the accumulation of metabolic intermediates and alteration of redox-sensitive pathways, affecting signalling pathways that further potentiate the inflammatory response. Importantly, the inflamed synovium is a multicellular tissue, with cells differing in their metabolic requirements depending on complex cell-cell interactions, nutrient supply, metabolic intermediates and transcriptional regulation. Therefore, understanding the complex interplay between metabolic and inflammatory pathways in synovial cells in RA will provide insight into the underlying mechanisms of disease pathogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.