ReviewCurrent rheumatology reports2010
Where do we stand with the genetics of psoriatic arthritis?
Review in Current rheumatology reports, 2010. 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, 9 citations in OpenAlex.
- A systems approach to renal inflammation in SLE.Clinical immunology (Orlando, Fla.) · 2017Review
- Gene expression differences between psoriasis patients with and without inflammatory arthritis.The Journal of investigative dermatology · 2015Article
- The perspective on psoriatic arthritis in Asia.Current rheumatology reports · 2011Review
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 at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Psoriasis and psoriatic arthritis (PsA) are interrelated heritable diseases. Polymorphisms in the genes encoded in the major histocompatibility complex region have consistently been associated with psoriasis and PsA and account for about 30% of the genetic risk. Recently, the results of multiple well-powered genome-wide association studies have identified several additional loci outside the major histocompatibility complex region associated with psoriasis risk, including three genes involved in interleukin (IL)-23 signaling (IL-23R, IL-23A, IL-12B), two genes that regulate nuclear factor-kappaB signaling (TNIP1, TNFAIP3), and two genes involved in the modulation of T-helper type 2 immune responses (IL-4, IL-13). These initial findings are beginning to illuminate the molecular pathways implicated in the pathogenesis of psoriasis and suggest priority targets for study in PsA cohorts. Of course, the next step will be to identify genetic risk factors specifically associated with PsA, and indeed, a formal genome-wide association study on PsA is being undertaken.
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.