ReviewArthritis research & therapy2009
Molecular therapies for systemic lupus erythematosus: clinical trials and future prospects.
Review in Arthritis research & therapy, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed.
- KS23, a novel peptide derived from adiponectin, inhibits retinal inflammation and downregulates the proportions of Th1 and Th17 cells during experimental autoimmune uveitis.Journal of neuroinflammation · 2019Article
- New Potential Pharmacological Functions of Chinese Herbal Medicines via Regulation of Autophagy.Molecules (Basel, Switzerland) · 2016Review
- Impact of loss of NF-κB1, NF-κB2 or c-REL on SLE-like autoimmune disease and lymphadenopathy in Fas(lpr/lpr) mutant mice.Immunology and cell biology · 2016Article
- The Role of Autophagy in Salivary Gland Homeostasis and Stress Responses.Journal of dental research · 2015Review
- Potential roles of nucleotide-binding oligomerization domain 2 in the pathogenesis of systemic lupus erythematosus.Rheumatology international · 2014Review
- Pharmacological regulators of autophagy and their link with modulators of lupus disease.British journal of pharmacology · 2014Review
- A novel NF-κB inhibitor, DHMEQ, ameliorates pristane-induced lupus in mice.Experimental and therapeutic medicine · 2014Article
- Article
- Phosphodiesterase 4-targeted treatments for autoimmune diseases.BMC medicine · 2013Review
- Generation of gene-engineered chimeric DNA molecules for specific therapy of autoimmune diseases.Human gene therapy methods · 2012Article
- Article
- Article
- Accelerated atherosclerosis in systemic lupus erythematosus: role of proinflammatory cytokines and therapeutic approaches.Journal of biomedicine & biotechnology · 2010Review
- Therapeutic strategies for SLE involving cytokines: mechanism-oriented therapies especially IFN-gamma targeting gene therapy.Journal of biomedicine & biotechnology · 2010Review
- Article
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
The prognosis of patients with systemic lupus erythematosus has greatly improved since treatment regimens combining corticosteroids and immunosuppressive medications have been widely adopted in therapeutic strategies given to these patients. Immune suppression is evidently efficient but also leads to higher susceptibility to infectious and malignant diseases. Toxic effects and sometimes unexpectedly dramatic complications of current therapies have been progressively reported. Identifying novel molecular targets therefore remains an important issue in the treatment of lupus. The aim of this review article is to highlight emerging pharmacological options and new therapeutic avenues for lupus with a particular focus on non-antibody molecular strategies.
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.