ArticleJournal of molecular and cellular cardiology2010
Uridine triphosphate (UTP) induces profibrotic responses in cardiac fibroblasts by activation of P2Y2 receptors.
Article in Journal of molecular and cellular cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 46 citations in OpenAlex.
- Cardiac function of colorectal cancer mice is remotely controlled by gut microbiota: regulating serum metabolites and myocardial cytokines.Animal microbiome · 2025Article
- Long noncoding RNA MALAT1 as a ceRNA drives mouse fibroblast activation via the miR-335-3p/P2ry2 axis.PloS one · 2024Article
- Therapeutic potential for P2YPurinergic signalling · 2023Review
- Article
- The Pleiotropic Role of Extracellular ATP in Myocardial Remodelling.Molecules (Basel, Switzerland) · 2023Review
- Discovery of Fungus-Derived Nornidulin as a Novel TMEM16A Inhibitor: A Potential Therapy to Inhibit Mucus Secretion in Asthma.Journal of experimental pharmacology · 2023Article
- Ectonucleoside triphosphate diphosphohydrolase-1 (CD39) impacts TGF-β1 responses: insights into cardiac fibrosis and function following myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2022Article
- Absence of P2YFrontiers in endocrinology · 2022Article
- P2Y2 promotes fibroblasts activation and skeletal muscle fibrosis through AKT, ERK, and PKC.BMC musculoskeletal disorders · 2021Article
- Role of Adenosine and Purinergic Receptors in Myocardial Infarction: Focus on Different Signal Transduction Pathways.Biomedicines · 2021Review
- Impaired UTP-induced relaxation in the carotid arteries of spontaneously hypertensive rats.Purinergic signalling · 2020Article
- Vascular endothelial growth factor-D mediates fibrogenic response in myofibroblasts.Molecular and cellular biochemistry · 2016Article
- Meningeal norepinephrine produces headache behaviors in rats via actions both on dural afferents and fibroblasts.Cephalalgia : an international journal of headache · 2015Article
- Targeted Disruption of Ig-Hepta/Gpr116 Causes Emphysema-like Symptoms That Are Associated with Alveolar Macrophage Activation.The Journal of biological chemistry · 2015Article
- Cardiac purinergic signalling in health and disease.Purinergic signalling · 2015Review
- Article
- Cellular mechanisms of tissue fibrosis. 6. Purinergic signaling and response in fibroblasts and tissue fibrosis.American journal of physiology. Cell physiology · 2014Review
- Uridine 5'-triphosphate promotes in vitro Schwannoma cell migration through matrix metalloproteinase-2 activation.PloS one · 2014Article
- Soluble ST2 and interleukin-33 levels in coronary artery disease: relation to disease activity and adverse outcome.PloS one · 2014Article
- Hydrolysis of extracellular ATP by ectonucleoside triphosphate diphosphohydrolase (ENTPD) establishes the set point for fibrotic activity of cardiac fibroblasts.The Journal of biological chemistry · 2013Article
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
Cardiac fibroblasts (CFs) play a key role in response to injury and remodeling of the heart. Nucleotide (P2) receptors regulate the heart but limited information is available regarding such receptors in CFs. We thus sought to determine if extracellular nucleotides regulate fibrotic responses (e.g., proliferation, migration and expression of profibrotic markers) of CFs in primary culture. UTP increased rat CF migration 3-fold (p<0.001), proliferation by 30% (p<0.05) and mRNA expression of profibrotic markers: alpha smooth muscle actin (alpha-SMA), plasminogen activator inhibitor-1 (PAI-1), transforming growth factor beta, soluble ST2, interleukin-6 and monocyte chemoattractant protein-1 (MCP-1) by 3.0-, 15-, 2.0-, 7.6-, 11-, and 6.1-fold, respectively (p<0.05). PAI-1 protein expression induced by UTP was dependent on protein kinase C (PKC) and extracellular signal-regulated kinase (ERK), based on blockade by the PKC inhibitor Ro-31-8220 and the ERK inhibitor U0126, respectively. The rank order for enhanced expression of PAI-1 and alpha-SMA by nucleotides (UTPgammaS>>UDPbetaS>>ATPgammaS), the expression of P2Y2 receptors as the most abundantly expressed P2Y receptor in rat CFs and a blunted response to UTP in P2Y2(-/-) mice all implicate P2Y2 as the predominant P2Y receptor that mediates nucleotide-promoted profibrotic responses. Additional results indicate that P2Y2 receptor-promoted profibrotic responses in CFs are transient, perhaps as a consequence of receptor desensitization. We conclude that P2Y2 receptor activation is profibrotic in CFs; thus inhibition of P2Y2 receptors may provide a novel means to diminish fibrotic remodeling and turnover of extracellular matrix in the heart.
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.