ReviewBritish journal of pharmacology2020
IL-11 in cardiac and renal fibrosis: Late to the party but a central player.
Review in British journal of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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
50 citing papers in PubMed, 90 citations in OpenAlex.
- Rehabilitation Training Can Significantly Increase the Serum IL-11 Levels and Improve the Prognosis in Ischemic Stroke Patients.Mediators of inflammation · 2023Trial
- Enhancing anti-fibrotic therapy: nanomedicine approaches to overcome current limitations.Materials today. Bio · 2026Review
- Induction of fibrosis in human kidney organoids delineates mechanisms and therapeutic targets of fibrotic kidney disease.Stem cell research & therapy · 2026Article
- Interleukin 11-Induced MicroRNAs as Functional Mediators and Circulating Biomarkers of Cardiac Fibrosis.Circulation research · 2026Article
- The role of IL-11 in chronic diseases.Frontiers in immunology · 2026Review
- Risk assessment of acute heart failure after endovascular therapy in acute ischemic stroke: a nomogram-based study.Frontiers in cardiovascular medicine · 2026Article
- Article
- Fibrosis: cross-organ biology and pathways to development of innovative drugs.Nature reviews. Drug discovery · 2025Review
- Interleukin 11 therapy causes acute left ventricular dysfunction.Cardiovascular research · 2024Article
- Macrophages in organ fibrosis: from pathogenesis to therapeutic targets.Cell death discovery · 2024Review
- Harnessing the regenerative potential of interleukin11 to enhance heart repair.Nature communications · 2024Article
- Characterization of the angiomodulatory effects of Interleukin 11 cis- and trans-signaling in the retina.Journal of neuroinflammation · 2024Article
- Research on key pathogenesis and potential intervention targets of idiopathic renal calculi composed of calcium oxalate (CaOx) based on bioinformatics.Translational andrology and urology · 2024Article
- Integrated analysis of endometrial stromal cell long noncoding RNA and mRNA expression profiles associated with TGF-β1-induced fibrosis.Acta biochimica et biophysica Sinica · 2024Article
- Harnessing the regenerative potential ofbioRxiv : the preprint server for biology · 2024Article
- Chronic Kidney Disease Diets for Kidney Failure Prevention: Insights from the IL-11 Paradigm.Nutrients · 2024Review
- The Influence of IL-11 on Cardiac Fibrosis in Experimental Models: A Systematic Review.Journal of cardiovascular development and disease · 2024Review
- Cardiac and Renal Fibrosis, the Silent Killer in the Cardiovascular Continuum: An Up-to-Date.Journal of cardiovascular development and disease · 2024Review
- Protective effect of UDCA against IL-11- induced cardiac fibrosis is mediated by TGR5 signalling.Frontiers in cardiovascular medicine · 2024Article
- Understanding interleukin 11 as a disease gene and therapeutic target.The Biochemical journal · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Fibrosis is a pathophysiological hallmark of cardiorenal disease. In the heart, fibrosis leads to contractile dysfunction and arrhythmias; in the kidney, it is the final common pathway for many diseases and predicts end-stage renal failure. Despite this, there are currently no specific anti-fibrotic treatments available for cardiac or renal disease. Recently and unexpectedly, IL-11 was found to be of major importance for cardiorenal fibroblast activation and fibrosis. In mouse models, IL-11 overexpression caused fibrosis of the heart and kidney while genetic deletion of Il11ra1 protected against fibrosis and preserved organ function. Neutralizing antibodies against IL-11 or IL-11RA have been developed that have anti-fibrotic activity in human fibroblasts and protect against fibrosis in murine models of disease. While IL-11 biology has been little studied and, we suggest, largely misunderstood, its autocrine activity in myofibroblasts appears non-redundant for fibrosis, which offers new opportunities to better understand and potentially target cardiorenal fibrosis.
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.