International Journal of Molecular Sciences

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Dear Colleagues,

Advances in the field of gastroenterology have led to elucidation and effective treatment of life-threatening diseases of the gastrointestinal tract, such as gastric cancers and colon cancers. On the other hand, disorders related to motility of the digestive tract are yet to be clarified. Although these diseases rarely result in fatal situations, they have a serious impact on patients’ quality of life; therefore, the importance of understanding them cannot be overemphasized.

There are efficient measures for investigating gastrointestinal motility, such as 24 h multichannel intraluminal impedance pH monitoring and high-resolution manometry, and careful analyses of the data obtained from these procedures contribute to the understanding of the physiology behind functional disorders of the alimentary tract. Furthermore, studies conducted with the aforementioned measures revealed the involvement of hypersensitivity in some functional diseases. At a molecular level, interstitial cells of Cajal, which are distributed within the muscle layers of the gastrointestinal tract, mediate the communication between autonomic nerve systems and the smooth muscle of the digestive tract, and the dysfunction of these cells is considered to be related to disorders of gastrointestinal motility.

In this Special Issue, we invite both clinical and basic research that will deepen our knowledge of diseases related to gastrointestinal motility and neurogastroenterology to better treat patients suffering from these diseases. Data on molecular mechanisms or pathophysiology are essential, and papers that only contain clinical trials/data are not acceptable.

Dr. Naoki Asano
Guest Editor

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Keywords

neurogastroenterology
gastrointestinal motility
gastroenterology

Published Papers (2 papers)

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Research

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9 pages, 1472 KiB

Open AccessArticle

The Impact of Duodenal Mucosal Vulnerability in the Development of Epigastric Pain Syndrome in Functional Dyspepsia

by Tomoki Okata, Kiyotaka Asanuma, Kenichiro Nakagawa, Waku Hatta, Tomoyuki Koike, Akira Imatani and Atsushi Masamune

Int. J. Mol. Sci. 2022, 23(22), 13947; https://doi.org/10.3390/ijms232213947 - 12 Nov 2022

Viewed by 1288

Abstract

An unidentified cause of functional dyspepsia (FD) is closely associated with medication resistance. Acid suppression is a traditional and preferential method for the treatment of FD, but the efficacy of this treatment varies between epigastric pain syndrome (EPS) and postprandial syndrome (PDS): it is efficient in the former but not much in the latter. Transepithelial electrical resistance (TEER), a surrogate of mucosal barrier function, was measured under pH 3 and pH 5 acidic conditions using duodenal biopsy specimens obtained from the patients with EPS and PDS and asymptomatic healthy controls. The infiltration of inflammatory cells to the duodenal mucosa was accessed by immunohistochemical analysis. The duodenal mucosal TEER in EPS patients was decreased by exposure to the acidic solution compared to that of the controls and the PDS patients. The decrease in TEER of the EPS patients was observed even under pH 5 weak acidic condition and was correlated to degree of the epigastric pain. Moreover, the duodenal mucosa of EPS patients presented an increase in mast cells and plasma cells that expressed Ig-E. Duodenal mucosal vulnerability to acid is likely to develop EPS. Full article

(This article belongs to the Special Issue Gastrointestinal Motility and Neurogastroenterology)

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Review

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21 pages, 2618 KiB

Open AccessReview

Clinical and Molecular Insights into Gastrointestinal Dysfunction in Myotonic Dystrophy Types 1 & 2

by Janel A. M. Peterson and Thomas A. Cooper

Int. J. Mol. Sci. 2022, 23(23), 14779; https://doi.org/10.3390/ijms232314779 - 26 Nov 2022

Cited by 1 | Viewed by 2756

Abstract

Myotonic dystrophy (DM) is a highly variable, multisystemic disorder that clinically affects one in 8000 individuals. While research has predominantly focused on the symptoms and pathological mechanisms affecting striated muscle and brain, DM patient surveys have identified a high prevalence for gastrointestinal (GI) symptoms amongst affected individuals. Clinical studies have identified chronic and progressive dysfunction of the esophagus, stomach, liver and gallbladder, small and large intestine, and rectum and anal sphincters. Despite the high incidence of GI dysmotility in DM, little is known regarding the pathological mechanisms leading to GI dysfunction. In this review, we summarize results from clinical and molecular analyses of GI dysfunction in both genetic forms of DM, DM type 1 (DM1) and DM type 2 (DM2). Based on current knowledge of DM primary pathological mechanisms in other affected tissues and GI tissue studies, we suggest that misregulation of alternative splicing in smooth muscle resulting from the dysregulation of RNA binding proteins muscleblind-like and CUGBP-elav-like is likely to contribute to GI dysfunction in DM. We propose that a combinatorial approach using clinical and molecular analysis of DM GI tissues and model organisms that recapitulate DM GI manifestations will provide important insight into defects impacting DM GI motility. Full article

(This article belongs to the Special Issue Gastrointestinal Motility and Neurogastroenterology)

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