ArticleFrontiers in physiology2013
Role of extracellular ATP and P2 receptor signaling in regulating renal cyst growth and interstitial inflammation in polycystic kidney disease.
Article in Frontiers in physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Role of abnormal energy metabolism in the progression of chronic kidney disease and drug intervention.Renal failure · 2022Article
- Modulation of P2XPhysiological reports · 2022Article
- Involvement of ceramide biosynthesis in increased extracellular vesicle release inFrontiers in endocrinology · 2022Article
- Extracellular Nucleotides and P2 Receptors in Renal Function.Physiological reviews · 2020Review
- Knockout ofAmerican journal of physiology. Renal physiology · 2019Article
- ATP release into ADPKD cysts via pannexin-1/P2X7 channels decreases ENaC activity.Biochemical and biophysical research communications · 2019Article
- Characterization of purinergic receptor expression in ARPKD cystic epithelia.Purinergic signalling · 2018Article
- P2Y2R is a direct target of HIF-1α and mediates secretion-dependent cyst growth of renal cyst-forming epithelial cells.Purinergic signalling · 2016Article
- Functional and therapeutic importance of purinergic signaling in polycystic kidney disease.American journal of physiology. Renal physiology · 2016Review
- The dark side of extracellular ATP in kidney diseases.Journal of the American Society of Nephrology : JASN · 2015Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polycystic kidney diseases (PKD) are a group of inherited ciliopathies in which the formation and growth of multiple cysts derived from the distal nephron and collecting duct leads to the disruption of normal kidney architecture, chronic interstitial inflammation/fibrosis and hypertension. Kidney failure is the most life-threatening complication of PKD, and is the consequence of cyst expansion, renal interstitial disease and loss of normal kidney tissue. Over the last decade, accumulating evidence suggests that the autocrine and paracrine effects of ATP (through its receptor family P2X and P2Y), could be detrimental for the progression of PKD. (2009). In vitro, ATP-P2 signaling promotes cystic epithelial cell proliferation, chloride-driven fluid secretion and apoptosis. Furthermore, dysfunction of the polycystin signal transduction pathways promotes the secretagogue activity of extracellular ATP by activating a calcium-activated chloride channel via purinergic receptors. Finally, ATP is a danger signal and could potentially contribute to interstitial inflammation associated with PKD. These data suggest that ATP-P2 signaling worsens the progression of cyst enlargement and interstitial inflammation in PKD.
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Registered trials
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