ArticleJournal of the American Society of Nephrology : JASN2016
Podocyte Purinergic P2X4 Channels Are Mechanotransducers That Mediate Cytoskeletal Disorganization.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 53 citations in OpenAlex.
- Inhibition of (interstitial) P2YPflugers Archiv : European journal of physiology · 2026Article
- Inhibition of (interstitial) P2YResearch square · 2026Article
- Podocyte-specific deletion of mechanochannel Piezo1 exacerbates proteinuria and podocyte injury in mouse hypertensive nephropathy.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Article
- Inhibition of (interstitial) P2YbioRxiv : the preprint server for biology · 2026Article
- Lysosome stress response and mitochondria injury are the earliest detectable alteration in FSGS.Scientific reports · 2025Article
- Mechanical Stress and Protective Mechanisms in Podocytes: Insights into Hypertensive Nephropathy.International journal of molecular sciences · 2025Review
- The intelligent podocyte: sensing and responding to a complex microenvironment.Nature reviews. Nephrology · 2025Review
- Revisiting nephrin signaling and its specialized effects on the uniquely adaptable podocyte.The Biochemical journal · 2025Review
- Piezo ion channels: long-sought-after mechanosensors mediating hypertension and hypertensive nephropathy.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Review
- Non-voltage-gated CaAmerican journal of physiology. Renal physiology · 2024Review
- Role of biophysics and mechanobiology in podocyte physiology.Nature reviews. Nephrology · 2024Review
- Roles of the mechanosensitive ion channel Piezo1 in the renal podocyte injury of experimental hypertensive nephropathy.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Article
- Vascular mechanotransduction.Physiological reviews · 2023Review
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- A protective role for <i>Drosophila</i> Filamin in nephrocytes via Yorkie mediated hypertrophy.Life science alliance · 2022Article
- Article
- Transient receptor potential cation channel 6 contributes to kidney injury induced by diabetes and hypertension.American journal of physiology. Renal physiology · 2022Article
- Characterization of purinergic receptor 2 signaling in podocytes from diabetic kidneys.iScience · 2021Article
- Review
- Resolving the Ionotropic P2X4 Receptor Mystery Points Towards a New Therapeutic Target for Cardiovascular Diseases.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Podocytes are specialized, highly differentiated epithelial cells in the kidney glomerulus that are exposed to glomerular capillary pressure and possible increases in mechanical load. The proteins sensing mechanical forces in podocytes are unconfirmed, but the classic transient receptor potential channel 6 (TRPC6) interacting with the MEC-2 homolog podocin may form a mechanosensitive ion channel complex in podocytes. Here, we observed that podocytes respond to mechanical stimulation with increased intracellular calcium concentrations and increased inward cation currents. However, TRPC6-deficient podocytes responded in a manner similar to that of control podocytes, and mechanically induced currents were unaffected by genetic inactivation of TRPC1/3/6 or administration of the broad-range TRPC blocker SKF-96365. Instead, mechanically induced currents were significantly decreased by the specific P2X purinoceptor 4 (P2X4) blocker 5-BDBD. Moreover, mechanical P2X4 channel activation depended on cholesterol and podocin and was inhibited by stabilization of the actin cytoskeleton. Because P2X4 channels are not intrinsically mechanosensitive, we investigated whether podocytes release ATP upon mechanical stimulation using a fluorometric approach. Indeed, mechanically induced ATP release from podocytes was observed. Furthermore, 5-BDBD attenuated mechanically induced reorganization of the actin cytoskeleton. Altogether, our findings reveal a TRPC channel-independent role of P2X4 channels as mechanotransducers in podocytes.
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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.