Evidence map›Paper›PMID 38252683›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2024

NHE3 inhibitor tenapanor maintains intestinal barrier function, decreases visceral hypersensitivity, and attenuates TRPV1 signaling in colonic sensory neurons.

Andrew J King, Lin Chang, Qian Li, Liansheng Liu, Yaohui Zhu, Pankaj J Pasricha, Ji Wang, Matthew Siegel, Jeremy S Caldwell, Susan Edelstein and 2 more

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
7.9field-weighted citation impact, top 2% of its field
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

15 citing papers in PubMed, 17 citations in OpenAlex.

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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

12 authors at 3 institutions in 1 country.

Andrew J KingArdelyx, Inc., Waltham, Massachusetts, United States.
Lin ChangGeffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States.
Qian LiDivision of Gastroenterology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States.
Liansheng LiuDivision of Gastroenterology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States.
Yaohui ZhuDivision of Gastroenterology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States.
Pankaj J PasrichaDivision of Gastroenterology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States.
Ji WangArdelyx, Inc., Waltham, Massachusetts, United States.
Matthew SiegelArdelyx, Inc., Waltham, Massachusetts, United States.
Jeremy S CaldwellArdelyx, Inc., Waltham, Massachusetts, United States.
Susan EdelsteinArdelyx, Inc., Waltham, Massachusetts, United States.
David P RosenbaumArdelyx, Inc., Waltham, Massachusetts, United States.
Kenji KozukaArdelyx, Inc., Waltham, Massachusetts, United States.ORCID 0009-0008-7243-6475
Ardelyx (United States) · USJohns Hopkins University · USUniversity of California, Los Angeles · US

Funding

Ardelyx, Inc.
6 · The paper itself

Abstract

The pathogenesis of irritable bowel syndrome (IBS) is multifactorial, characterized in part by increased intestinal permeability, and visceral hypersensitivity. Increased permeability is associated with IBS severity and abdominal pain. Tenapanor is FDA-approved for the treatment of IBS with constipation (IBS-C) and has demonstrated improvements in bowel motility and a reduction in IBS-related pain; however, the mechanism by which tenapanor mediates these functions remains unclear. Here, the effects of tenapanor on colonic pain signaling and intestinal permeability were assessed through behavioral, electrophysiological, and cell culture experiments. Intestinal motility studies in rats and humans demonstrated that tenapanor increased luminal sodium and water retention and gastrointestinal transit versus placebo. A significantly reduced visceral motor reflex (VMR) to colonic distension was observed with tenapanor treatment versus vehicle in two rat models of visceral hypersensitivity (neonatal acetic acid sensitization and partial restraint stress; both

Indexed as

Irritable Bowel SyndromeIsoquinolinesSulfonamidesAbdominal PainAnimalsCapsaicinColonCytokinesHumansIntestinal Barrier FunctionRatsSensory Receptor CellsSodium-Hydrogen Exchanger 3TRPV Cation ChannelsCapsaicinCytokinesIsoquinolinesSodium-Hydrogen Exchanger 3SulfonamidestenapanorTRPV1 protein, humanTRPV Cation Channelsdorsal root ganglia neuronsintestinal barrier permeabilitytenapanorTRPV1visceral hypersensitivity

Identifiers

PMID38252683
PMCPMC11376972
OpenAlexW4391093885

What OpenQuestion 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 OpenQuestion graph.