ReviewJournal of inflammation research2026
"Gut-Joint Axis" Perspective on Immunometabolic Crosstalk in Osteoarthritis: A Narrative Review of Mechanistic Insights and Targeted Strategies.
Review in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is a heterogeneous whole-joint disease in which local mechanical injury interacts with systemic metabolic dysfunction and chronic low-grade inflammation. Increasing evidence links gut microbiota dysbiosis to OA, but the mechanisms through which gut-derived perturbations contribute to joint structural damage remain incompletely integrated. This narrative review synthesizes clinical and experimental evidence on the gut-joint axis, focusing on a mechanistic sequence in which dysbiosis impairs intestinal barrier integrity, increases systemic exposure to gut-derived inflammatory signals, activates pattern-recognition receptor (PRR) signaling, and induces immunometabolic reprogramming in joint-resident cells. This process may amplify synovial inflammation, cartilage catabolism, and subchondral bone remodeling, thereby contributing to structural degeneration. Unlike previous reviews that primarily summarize microbiota-associated alterations or individual interventions, this review positions immunometabolic reprogramming as the mechanistic bridge between gut-derived inflammatory inputs and local joint degeneration. We further discuss therapeutic opportunities targeting microbiota homeostasis, intestinal barrier repair, inflammatory amplification, immunometabolic pathways, and natural products and phytochemicals. Overall, the gut-joint axis is best viewed as an amplifier of inflammatory and metabolic susceptibility rather than an independent initiator of OA. This framework may support biomarker-guided stratification and targeted interventions for metabolically driven OA.
Indexed as
Identifiers
What OpenQuestion holds
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.