Evidence map›Paper›PMID 42117913›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026

HIF-Regulated Pannexin-1 Channel Drives Luminal ATP Accumulation in Kidney Cysts.

Kathrin Skoczynski, Julia Katharina Scholz, Raluca Ursu, Johannes Schödel, Steffen Grampp, Stephanie Naas, Victoria Lauer, Mario Schiffer, Maike Büttner-Herold, Bjoern Buchholz and 1 more

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Kathrin SkoczynskiDepartment of Physiology I, Institute of Physiology, University of Regensburg, Regensburg, Germany.
Julia Katharina ScholzDepartment of Internal Medicine 5-Hematology and Oncology, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) and University Hospital, Erlangen, Germany.
Raluca UrsuDepartment of Nephrology and Hypertension, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) and University Hospital, Erlangen, Germany.
Johannes SchödelDepartment of Nephrology and Hypertension, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) and University Hospital, Erlangen, Germany.
Steffen GramppDepartment of Nephrology and Hypertension, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) and University Hospital, Erlangen, Germany.
Stephanie NaasDepartment of Nephrology and Hypertension, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) and University Hospital, Erlangen, Germany.
Victoria LauerDepartment of Nephrology and Hypertension, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) and University Hospital, Erlangen, Germany.
Mario SchifferDepartment of Nephrology and Hypertension, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) and University Hospital, Erlangen, Germany.
Maike Büttner-HeroldDepartment of Nephropathology, Institute of Pathology, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) and University Hospital, Erlangen, Germany.
Bjoern BuchholzDepartment of Physiology I, Institute of Physiology, University of Regensburg, Regensburg, Germany.
Andre KrausDepartment of Nephrology and Hypertension, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) and University Hospital, Erlangen, Germany.

Funding

Deutsche Forschungsgemeinschaft (DFG) 509149993
6 · The paper itself

Abstract

Autosomal dominant polycystic kidney disease (ADPKD) is marked by the progressive development of bilateral kidney cysts, leading to compression of intact surrounding tissue and a subsequent decline in kidney function. Accumulation of ATP within the cyst fluid significantly drives cyst expansion by activating purinergic receptors, thereby promoting calcium-dependent chloride secretion. Moreover, the induction of hypoxia-inducible factor 1α (HIF-1α) in cyst-lining epithelial cells further enhances chloride conductance. However, the mechanisms underlying ATP release into the cyst fluid and the role of HIF-1α in cyst enlargement remain incompletely understood. Here, we demonstrate that the ATP-release channel Pannexin-1 is regulated by HIF-1α in kidney tubular cells, leading to its prominent localization at the apical membrane of kidney cysts in both human and murine ADPKD kidney tissue. Apical ATP release is elevated in PKD1-deficient cyst-forming cells following pharmacological induction of HIF-1α and attenuated by two Pannexin-1 inhibitors, Probenecid and Brilliant Blue FCF (BB-FCF). HIF-dependent cyst growth in vitro is inhibited by basolateral application of the cell-permeable Probenecid, whereas the cell-impermeable BB-FCF requires luminal application to exert its effect. In conclusion, HIF-1α promotes Pannexin-1 expression in cyst-lining cells, facilitating directional ATP release into the cyst lumen and driving ATP-dependent cyst expansion.

Indexed as

Adenosine TriphosphateConnexinsHypoxia-Inducible Factor 1, alpha SubunitNerve Tissue ProteinsPolycystic Kidney, Autosomal DominantAnimalsHumansMiceAdenosine TriphosphateConnexinsHIF1A protein, humanHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitNerve Tissue ProteinsPANX1 protein, humanPanx1 protein, mouseATPcyst growthHIF‐1αPannexin‐1polycystic kidney disease

Identifiers

PMID42117913
PMCPMC13164829

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.