ArticleArthritis & rheumatology (Hoboken, N.J.)2026
Dual Action of Dipyridamole in Experimental Rheumatoid Arthritis: Suppression of Joint Inflammation and Upregulation of Muscle Anabolism via Adenosine and AMPK Pathways.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- Immunometabolic and translational considerations of dipyridamole in experimental rheumatoid arthritis: comment on the article by Marco-Bonilla et al.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- Reply.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- Neutrophil percentage-to-albumin ratio is associated with low muscle mass risk in rheumatoid arthritis: evidence from a hospital-based cohort and NHANES validation.Frontiers in immunology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
objectiveRheumatoid sarcopenia, characterized by the progressive loss of skeletal muscle mass and function, is a frequent comorbidity in rheumatoid arthritis (RA), linked to prolonged, severe systemic inflammation. Purinergic signaling (adenosine, AMP, and ATP) plays a crucial role in inflammation, myogenesis, and muscle hypertrophy. Dipyridamole, an antiplatelet agent, enhances extracellular adenosine availability, alters AMP/ATP ratio, and activates A2BR and AMP kinase (AMPK) pathways. We aim to investigate its potential use as a therapeutic agent for RA and rheumatoid sarcopenia.
methodsK/BxN-induced mice received preventive or therapeutic dipyridamole treatment daily and were sacrificed at joint inflammation peak and resolution stage. Motor activity tests and dual-energy x-ray absorptiometry were performed. C-reactive protein levels were also analyzed in serum, and cytokines array was performed in serum and muscle. Histology of tibialis anterior and talus joint were studied. Myogenesis, purinergic system, atrophy, and senescence key markers were analyzed via Western blot and reverse transcriptase-polymerase chain reaction in gastrocnemius. Nucleotide content via high-performance liquid chromatography was performed. Two-dimensional and three-dimensional models with C2C12 cells were done.
resultsDipyridamole reduced joint, muscle, and systemic inflammation, counteracting muscle wasting and physical inactivity via an anabolic mechanism involving down-regulation of myostatin expression. This effect was mediated by increased adenosine and AMP levels, which activate adenosine A2BR and downstream cAMP/AMPK signaling pathways.
conclusionThese results support a dual role for dipyridamole in RA, combining robust anti-inflammatory effects with a novel, myostatin-linked anabolic action on sarcopenia, mediated through adenosine and AMPK signaling, distinct from conventional therapeutic mechanisms.
Indexed as
Identifiers
What Socratic 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 Socratic graph.