ReviewNeurogastroenterology and motility2010
Ion channel remodeling in gastrointestinal inflammation.
Review in Neurogastroenterology and motility, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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
20 citing papers in PubMed, 42 citations in OpenAlex.
- Pharmacological Activation of TRPC6 Channel Prevents Colitis Progression.International journal of molecular sciences · 2024Article
- Neuroimmune interplay in kidney health and disease: Role of renal nerves.Autonomic neuroscience : basic & clinical · 2023Review
- Exogenous H2S promotes ion channel reconstruction to regulate colonic motility in rats with dinitrobenzene sulfonic acid-induced colitis.Annals of translational medicine · 2022Article
- The potential ofRSC advances · 2019Article
- In Silico Evaluation of Ibuprofen and Two Benzoylpropionic Acid Derivatives with Potential Anti-Inflammatory Activity.Molecules (Basel, Switzerland) · 2019Article
- Regulation of platelet-activating factor-mediated protein tyrosine phosphatase 1B activation by a Janus kinase 2/calpain pathway.PloS one · 2017Article
- Electrophysiological Mechanisms of Gastrointestinal Arrhythmogenesis: Lessons from the Heart.Frontiers in physiology · 2016Review
- Mechanisms of Electrical Activation and Conduction in the Gastrointestinal System: Lessons from Cardiac Electrophysiology.Frontiers in physiology · 2016Review
- Interaction between hydrogen sulfide-induced sulfhydration and tyrosine nitration in the KATP channel complex.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- Real-time measurement of biomagnetic vector fields in functional syncytium using amorphous metal.Scientific reports · 2015Article
- Colitis-induced neuroplasticity disrupts motility in the inflamed and post-inflamed colon.The Journal of clinical investigation · 2015Review
- Postranslational Modification of Ion Channels in Colonic Inflammation.Current neuropharmacology · 2015Review
- Voltage dependent potassium channel remodeling in murine intestinal smooth muscle hypertrophy induced by partial obstruction.PloS one · 2014Article
- Changes in the expression of smooth muscle contractile proteins in TNBS- and DSS-induced colitis in mice.Inflammation · 2013Article
- Spatial analysis of slowly oscillating electric activity in the gut of mice using low impedance arrayed microelectrodes.PloS one · 2013Article
- Hydrogen sulfide as an allosteric modulator of ATP-sensitive potassium channels in colonic inflammation.Molecular pharmacology · 2013Article
- Nicotine suppresses hyperexcitability of colonic sensory neurons and visceral hypersensivity in mouse model of colonic inflammation.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Targeting ion channels for the treatment of gastrointestinal motility disorders.Therapeutic advances in gastroenterology · 2012Article
- Orexins stimulate the 'appetite' of the gut.The Journal of physiology · 2011Article
- Can the intestinal dysmotility of critical illness be differentiated from postoperative ileus?Current gastroenterology reports · 2011Review
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
backgroundGastrointestinal inflammation significantly affects the electrical excitability of smooth muscle cells. Considerable progress over the last few years have been made to establish the mechanisms by which ion channel function is altered in the setting of gastrointestinal inflammation. Details have begun to emerge on the molecular basis by which ion channel function may be regulated in smooth muscle following inflammation. These include changes in protein and gene expression of the smooth muscle isoform of L-type Ca(2+) channels and ATP-sensitive K(+) channels. Recent attention has also focused on post-translational modifications as a primary means of altering ion channel function in the absence of changes in protein/gene expression. Protein phosphorylation of serine/theronine or tyrosine residues, cysteine thiol modifications, and tyrosine nitration are potential mechanisms affected by oxidative/nitrosative stress that alter the gating kinetics of ion channels. Collectively, these findings suggest that inflammation results in electrical remodeling of smooth muscle cells in addition to structural remodeling. PURPOSE: The purpose of this review is to synthesize our current understanding regarding molecular mechanisms that result in altered ion channel function during gastrointestinal inflammation and to address potential areas that can lead to targeted new therapies.
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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.