SynthesisRheumatology international2026
PARP1 as a novel therapeutic and diagnostic tool in autoimmune rheumatic diseases: a systematic literature review.
Synthesis in Rheumatology international, 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ADP-ribosylation is a reversible post-translational modification regulated by poly(ADP-ribose) polymerases (PARPs), a family of enzymes involved in DNA repair, transcriptional regulation, and immune responses. Among the 17 known PARP family members, PARP1 is the most extensively studied in autoimmune rheumatic diseases (ARDs). Although increasing evidence implicates PARP1 in ARD pathogenesis, its potential diagnostic and therapeutic relevance has not been systematically synthesised. This systematic literature review (SLR) aimed to evaluate the role of PARP1 in the pathogenesis, diagnosis and treatment of ARDs. MEDLINE and Embase databases were searched on 6th May 2026 using MeSH keywords for systemic ARDs, PARP1 and PARP inhibitors. Studies involving adult ARD patients and relevant animal models were included. Of 3564 records identified (post-deduplication), 41 studies were included. Seventeen studies included human ARD cohorts and nine used murine models recapitulating specific ARDs. Most studies focused on systemic lupus erythematosus (SLE; n = 18), rheumatoid arthritis (n = 14), and systemic sclerosis (SSc; n = 7). Across experimental models, inhibition or genetic disruption of PARP1 frequently attenuated inflammatory responses, reducing pro-inflammatory mediator expression, oxidative stress, and tissue damage. However, PARP1 also demonstrated context-dependent regulatory effects in immune signalling pathways. In SLE and SSc, reduced PARP1 activity and impaired DNA repair capacity were reported. Genetic association studies produced heterogeneous findings, while several studies identified PARP1-related autoantibodies or activity changes as potential diagnostic biomarkers, particularly in SLE. Overall, our SLR highlights PARP1 as an important regulator of immune pathways in ARDs, with potential relevance for future diagnostic and therapeutic strategies. PROSPERO: CRD420251000954.
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.