ReviewCurrent rheumatology reports2013
Scleroderma-related lung disease: are adipokines involved pathogenically?
Review in Current rheumatology reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 9 citations in OpenAlex.
- Circulating Adipokines as Diagnostic and Prognostic Markers in Idiopathic Pulmonary Fibrosis.Lung · 2026Article
- Peripheral Biomarker Signatures in Rheumatoid Arthritis-Associated Interstitial Lung Disease.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- Association Between Visceral Adipose Tissue and Chronic Respiratory Diseases: A Two-Sample Multivariable Mendelian Randomization Study in European Population.International journal of chronic obstructive pulmonary disease · 2025Article
- Linking Adiposity to Interstitial Lung Disease: The Role of the Dysfunctional Adipocyte and Inflammation.Cells · 2023Review
- Diagnosis of Fibrotic Hypersensitivity Pneumonitis: Is There a Role for Biomarkers?Life (Basel, Switzerland) · 2023Review
- Role of adipokines in systemic sclerosis pathogenesis.European journal of rheumatology · 2020Review
- Analysis of serum adiponectin and leptin in patients with acute exacerbation of idiopathic pulmonary fibrosis.Scientific reports · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Scleroderma is a systemic autoimmune disease of unknown etiology whose characteristic features include endothelial cell dysfunction, fibroblast proliferation, and immune dysregulation. Although almost any organ can be pathologically involved in scleroderma, lung complications including interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH) are the leading cause of death in patients with this condition. Currently, the molecular mechanisms leading to development of scleroderma-related lung disease are poorly understood; however, the systemic nature of this condition has led many to implicate circulating factors in the pathogenesis of some of its organ impairment. In this article we focus on a new class of circulating factors derived from adipose-tissue called adipokines, which are known to be altered in scleroderma. Recently, the adipokines adiponectin and leptin have been found to regulate biological activity in endothelial, fibroblast, and immune cell types in lung and in many other tissues. The pleiotropic nature of these circulating factors and their functional activity on many cell types implicated in the pathogenesis of ILD and PAH suggest these hormones may be mechanistically involved in the onset and/or progression of scleroderma-related lung diseases.
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.