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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (15 November 2023) | Viewed by 23446

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Dr. Kulmira Nurgali

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1. Institute for Health and Sport, Victoria University, Melbourne 3011, Australia
2. Department of Medicine Western Health, University of Melbourne, Melbourne 3010, Australia
3. Regenerative Medicine and Stem Cells Program, Australian Institute of Musculoskeletal Sciences, Melbourne 3021, Australia
Interests: development of novel therapies for the treatment of enteric neuropathy; gut–brain axis; inflammatory bowel disease; colorectal cancer; gastrointestinal side effects of chemotherapy
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Dr. Ainsley Robinson

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1. Institute for Health and Sport, Victoria University, Melbourne 3011, Australia
2. Research and Ethics Department, Goulburn Valley Health, Shepparton 3630, Australia
3. School of Rural Health, La Trobe University, Mildura 3520, Australia
Interests: enteric nervous system; mesenchymal stem-cell-based treatments; inflammatory bowel disease; enteric neuropathy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Recent technological advances unravel many molecular, cellular, genetic, immunological, and microbiological aspects of the gastrointestinal tract functions in health and disease. These discoveries have important implications for a better understanding of basic mechanisms that maintain the physiological homeostasis of the gut. Malfunctioning of these fine-tuned molecular mechanisms leads to the onset and progression of gastrointestinal disorders. Understanding the molecular mechanisms and pathways is the turning point toward the development of novel diagnostic approaches and therapies for gastrointestinal disorders. Led by Prof Kulmira Nurgali and Dr Ainsley Robinson and assisted by our promotion editor, Dr Nyanbol Kuol (University of Nevada, Reno, US), this Special Issue of IJMS, “Molecular Research of Gastrointestinal Disease”, welcomes basic and clinical original research and review papers to be submitted for peer review. The submitted papers can cover any aspects of molecular research relevant to a broad range of gastrointestinal disorders.

Topics of interest include but are not limited to:

molecular mechanisms of gastrointestinal functions in health and disease;
molecular targets for therapeutic intervention;
molecular markers for diagnostics of gastrointestinal disorders.

Dr. Kulmira Nurgali
Dr. Ainsley Robinson
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

gastrointestinal health
gastrointestinal disorders
gastrointestinal disease
gastrointestinal homeostasis
molecular targets
mechanisms
pathways
molecular markers
therapeutic targets

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Molecular Research of Gastrointestinal Disease 2.0 in International Journal of Molecular Sciences (5 articles)

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Research

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13 pages, 5457 KiB

Open AccessArticle

Does Telotristat Have a Role in Preventing Carcinoid Heart Disease?

by Aura D. Herrera-Martínez, Antonio C. Fuentes-Fayos, Rafael Sanchez-Sanchez, Antonio J. Montero, André Sarmento-Cabral, María A. Gálvez-Moreno, Manuel D. Gahete and Raúl M. Luque

Int. J. Mol. Sci. 2024, 25(4), 2036; https://doi.org/10.3390/ijms25042036 - 7 Feb 2024

Viewed by 1404

Abstract

Carcinoid heart disease (CHD) is a frequent and life-threatening complication in patients with carcinoid tumors. Its clinical management is challenging is some cases since serotonin-induced valve fibrosis leads to heart failure. Telotristat is an inhibitor of tryptophan-hydroxylase (TPH), a key enzyme in serotonin production. Telotristat use in patients with carcinoid syndrome and uncontrollable diarrhea under somatostatin analogs is approved, but its specific role in patients with CHD is still not clear. IN this context, we aimed to explore the effect of telotristat in heart fibrosis using a mouse model of serotonin-secreting metastasized neuroendocrine neoplasm (NEN). To this aim, four treatment groups (n = 10/group) were evaluated: control, monthly octreotide, telotristat alone, and telotristat combined with octreotide. Plasma serotonin and NT-proBNP levels were determined. Heart fibrosis was histologically evaluated after 6 weeks of treatment or when an individual mouse’s condition was close to being terminal. Heart fibrosis was observed in all groups. Non-significant reductions in primary tumor growth were observed in all of the treated groups. Feces volume was increased in all groups. A non-significant decrease in feces volume was observed in the octreotide or telotristat-treated groups, while it was significantly reduced with the combined treatment at the end of the study compared with octreotide (52 g reduction; p < 0.01) and the control (44.5 g reduction; p = 0.05). Additionally, plasma NT-proBNP decreased in a non-significant, but clinically relevant, manner in the octreotide (28.2% reduction), telotristat (45.9% reduction), and the octreotide + telotristat (54.1% reduction) treatment groups. No significant changes were observed in plasma serotonin levels. A similar non-significant decrease in heart valve fibrosis was observed in the three treated groups. In conclusion, Telotristat alone and especially in combination with octreotide decreases NT-proBNP levels in a mouse model of serotonin-secreting metastasized NEN, when compared with the control and octreotide, but its effect on heart valve fibrosis (alone and in combination) was not superior to octreotide in monotherapy. Full article

(This article belongs to the Special Issue Molecular Research of Gastrointestinal Disease)

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19 pages, 4179 KiB

Open AccessArticle

Faster Gastrointestinal Transit, Reduced Small Intestinal Smooth Muscle Tone and Dysmotility in the Nlgn3^R451C Mouse Model of Autism

by Suzanne Hosie, Tanya Abo-Shaban, Kevin Mou, Gayathri K. Balasuriya, Mitra Mohsenipour, Mohammed U. Alamoudi, Rhiannon T. Filippone, Gabrielle T. Belz, Ashley E. Franks, Joel C. Bornstein, Kulmira Nurgali and Elisa L. Hill-Yardin

Int. J. Mol. Sci. 2024, 25(2), 832; https://doi.org/10.3390/ijms25020832 - 9 Jan 2024

Viewed by 1802

Abstract

Individuals with autism often experience gastrointestinal issues but the cause is unknown. Many gene mutations that modify neuronal synapse function are associated with autism and therefore may impact the enteric nervous system that regulates gastrointestinal function. A missense mutation in the Nlgn3 gene encoding the cell adhesion protein Neuroligin-3 was identified in two brothers with autism who both experienced severe gastrointestinal dysfunction. Mice expressing this mutation (Nlgn3^R451C mice) are a well-studied preclinical model of autism and show autism-relevant characteristics, including impaired social interaction and communication, as well as repetitive behaviour. We previously showed colonic dysmotility in response to GABAergic inhibition and increased myenteric neuronal numbers in the small intestine in Nlgn3^R451C mice bred on a mixed genetic background. Here, we show that gut dysfunction is a persistent phenotype of the Nlgn3 R451C mutation in mice backcrossed onto a C57BL/6 background. We report that Nlgn3^R451C mice show a 30.9% faster gastrointestinal transit (p = 0.0004) in vivo and have 6% longer small intestines (p = 0.04) compared to wild-types due to a reduction in smooth muscle tone. In Nlgn3^R451C mice, we observed a decrease in resting jejunal diameter (proximal jejunum: 10.6% decrease, p = 0.02; mid: 9.8%, p = 0.04; distal: 11.5%, p = 0.009) and neurally regulated dysmotility as well as shorter durations of contractile complexes (mid: 25.6% reduction in duration, p = 0.009; distal: 30.5%, p = 0.004) in the ileum. In Nlgn3^R451C mouse colons, short contractions were inhibited to a greater extent (57.2% by the GABA_A antagonist, gabazine, compared to 40.6% in wild-type mice (p = 0.007). The inhibition of nitric oxide synthesis decreased the frequency of contractile complexes in the jejunum (WT p = 0.0006, Nlgn3^R451C p = 0.002), but not the ileum, in both wild-type and Nlgn3^R451C mice. These findings demonstrate that changes in enteric nervous system function contribute to gastrointestinal dysmotility in mice expressing the autism-associated R451C missense mutation in the Neuroligin-3 protein. Full article

(This article belongs to the Special Issue Molecular Research of Gastrointestinal Disease)

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24 pages, 18429 KiB

Open AccessArticle

Complement C3-Deficiency-Induced Constipation in FVB/N-C3^em1Hlee/Korl Knockout Mice Was Significantly Relieved by Uridine and Liriope platyphylla L. Extracts

by Hee-Jin Song, Ji-Eun Kim, You-Jeong Jin, Yu-Jeong Roh, Ayun Seol, Tae-Ryeol Kim, Ki-Ho Park, Eun-Seo Park, Beum-Soo An, Seung-Yun Yang, Sungbaek Seo, Seong-Min Jo, Young-Suk Jung and Dae-Youn Hwang

Int. J. Mol. Sci. 2023, 24(21), 15757; https://doi.org/10.3390/ijms242115757 - 30 Oct 2023

Cited by 1 | Viewed by 1502

Abstract

Complement component 3 (C3) deficiency has recently been known as a cause of constipation, without studies on the therapeutic efficacy. To evaluate the therapeutic agents against C3-deficiency-induced constipation, improvements in the constipation-related parameters and the associated molecular mechanisms were examined in FVB/N-C3^em1Hlee/Korl knockout (C3 KO) mice treated with uridine (Urd) and the aqueous extract of Liriope platyphylla L. (AEtLP) with laxative activity. The stool parameters and gastrointestinal (GI) transit were increased in Urd- and AEtLP-treated C3 KO mice compared with the vehicle (Veh)-treated C3 KO mice. Urd and AEtLP treatment improved the histological structure, junctional complexes of the intestinal epithelial barrier (IEB), mucin secretion ability, and water retention capacity. Also, an improvement in the composition of neuronal cells, the regulation of excitatory function mediated via the 5-hydroxytryptamine (5-HT) receptors and muscarinic acetylcholine receptors (mAChRs), and the regulation of the inhibitory function mediated via the neuronal nitric oxide synthase (nNOS) and inducible NOS (iNOS) were detected in the enteric nervous system (ENS) of Urd- and AEtLP-treated C3 KO mice. Therefore, the results of the present study suggest that C3-deficiency-induced constipation can improve with treatment with Urd and AEtLP via the regulation of the mucin secretion ability, water retention capacity, and ENS function. Full article

(This article belongs to the Special Issue Molecular Research of Gastrointestinal Disease)

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18 pages, 7802 KiB

Open AccessArticle

Interleukin-13 Mediates Non-Steroidal Anti-Inflammatory-Drug-Induced Small Intestinal Mucosal Injury with Ulceration

by Rei Kawashima, Shun Tamaki, Yusuke Hara, Tatsunori Maekawa, Fumitaka Kawakami and Takafumi Ichikawa

Int. J. Mol. Sci. 2023, 24(19), 14971; https://doi.org/10.3390/ijms241914971 - 7 Oct 2023

Cited by 3 | Viewed by 1529

Abstract

Non-steroidal anti-inflammatory drugs (NSAIDs), which are antipyretics and analgesics, cause gastrointestinal disorders, such as inflammation and ulcers. To prescribe NSAIDs more safely, it is important to clarify the mechanism of NSAID-induced gastrointestinal mucosal injury. However, there is a paucity of studies on small intestinal mucosal damage by NSAIDs, and it is currently unknown whether inflammation and ulceration also occur in the small intestine, and whether mediators are involved in the mechanism of injury. Therefore, in this study, we created an animal model in which small intestinal mucosal injury was induced using NSAIDs (indomethacin; IDM). Focusing on the dynamics of immune regulatory factors related to the injury, we aimed to elucidate the pathophysiological mechanism involved. We analyzed the pathological changes in the small intestine, the expression of immunoregulatory factors (cytokines), and identified cytokine secretion and expression cells from isolated lamina propria mononuclear cells (LPMCs). Ulcers were formed in the small intestine by administering IDM. Although the mRNA expression levels of IL-1β, IL-6, and TNFα were decreased on day 7 after IDM administration, IL-13 mRNA levels increased from day 3 after IDM administration and remained high even on day 7. The IL-13 mRNA expression and the secretion of IL-13 were increased in small intestinal LPMCs isolated from the IDM-treated group. In addition, we confirmed that IL-13 was expressed in CD4-positive T cells. These results provided new evidence that IL-13 production from CD4-positive T cells in the lamina propria of the small intestine contributes to NSAID-induced mucosal injury. Full article

(This article belongs to the Special Issue Molecular Research of Gastrointestinal Disease)

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12 pages, 1950 KiB

Open AccessArticle

LIX1 Controls MAPK Signaling Reactivation and Contributes to GIST-T1 Cell Resistance to Imatinib

by Salomé Ruiz-Demoulin, Eva Trenquier, Sanaa Dekkar, Sébastien Deshayes, Prisca Boisguérin, César Serrano, Pascal de Santa Barbara and Sandrine Faure

Int. J. Mol. Sci. 2023, 24(8), 7138; https://doi.org/10.3390/ijms24087138 - 12 Apr 2023

Cited by 6 | Viewed by 2248

Abstract

Gastrointestinal stromal tumor (GIST), the most common sarcoma, is mainly caused by an oncogenic mutation in the KIT receptor tyrosine kinase. Targeting KIT using tyrosine kinase inhibitors, such as imatinib and sunitinib, provides substantial benefit; however, in most patients, the disease will eventually progress due to KIT secondary mutations leading to treatment failure. Understanding how GIST cells initially adapt to KIT inhibition should guide the selection of appropriate therapies to overcome the emergence of resistance. Several mechanisms have been broadly implicated in the resistance to imatinib anti-tumoral effects, including the reactivation of MAPK signaling upon KIT/PDGFRA targeted inhibition. This study provides evidence that LImb eXpression 1 (LIX1), a protein we identified as a regulator of the Hippo transducers YAP1 and TAZ, is upregulated upon imatinib or sunitinib treatment. LIX1 silencing in GIST-T1 cells impaired imatinib-induced MAPK signaling reactivation and enhanced imatinib anti-tumor effect. Our findings identified LIX1 as a key regulator of the early adaptative response of GIST cells to targeted therapies. Full article

(This article belongs to the Special Issue Molecular Research of Gastrointestinal Disease)

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16 pages, 1359 KiB

Open AccessArticle

Pravastatin Improves Colonic and Hepatic Microcirculatory Oxygenation during Sepsis without Affecting Mitochondrial Function and ROS Production in Rats

by Anne Kuebart, Katharina Gross, Jan-Joschua Ripkens, Theresa Tenge, Annika Raupach, Jan Schulz, Richard Truse, Stefan Hof, Carsten Marcus, Christian Vollmer, Inge Bauer, Olaf Picker and Anna Herminghaus

Int. J. Mol. Sci. 2023, 24(6), 5455; https://doi.org/10.3390/ijms24065455 - 13 Mar 2023

Cited by 3 | Viewed by 2007

Abstract

Microcirculatory and mitochondrial dysfunction are considered the main mechanisms of septic shock. Studies suggest that statins modulate inflammatory response, microcirculation, and mitochondrial function, possibly through their action on peroxisome proliferator-activated receptor alpha (PPAR-α). The aim of this study was to examine the effects of pravastatin on microcirculation and mitochondrial function in the liver and colon and the role of PPAR-α under septic conditions. This study was performed with the approval of the local animal care and use committee. Forty Wistar rats were randomly divided into 4 groups: sepsis (colon ascendens stent peritonitis, CASP) without treatment as control, sepsis + pravastatin, sepsis + PPAR-α-blocker GW6471, and sepsis + pravastatin + GW6471. Pravastatin (200 µg/kg s.c.) and GW6471 (1 mg/kg) were applied 18 h before CASP-operation. 24 h after initial surgery, a relaparotomy was performed, followed by a 90 min observation period for assessment of microcirculatory oxygenation (μHbO₂) of the liver and colon. At the end of the experiments, animals were euthanized, and the colon and liver were harvested. Mitochondrial function was measured in tissue homogenates using oximetry. The ADP/O ratio and respiratory control index (RCI) for complexes I and II were calculated. Reactive oxygen species (ROS) production was assessed using the malondialdehyde (MDA)-Assay. Statistics: two-way analysis of variance (ANOVA) + Tukey’s/Dunnett’s post hoc test for microcirculatory data, Kruskal–Wallis test + Dunn’s post hoc test for all other data. In control septic animals µHbO₂ in liver and colon deteriorated over time (µHbO₂: −9.8 ± 7.5%* and −7.6 ± 3.3%* vs. baseline, respectively), whereas after pravastatin and pravastatin + GW6471 treatment μHbO₂ remained constant (liver: µHbO₂ pravastatin: −4.21 ± 11.7%, pravastatin + GW6471: −0.08 ± 10.3%; colon: µHbO₂ pravastatin: −0.13 ± 7.6%, pravastatin + GW6471: −3.00 ± 11.24%). In both organs, RCI and ADP/O were similar across all groups. The MDA concentration remained unchanged in all groups. Therefore, we conclude that under septic conditions pravastatin improves microcirculation in the colon and liver, and this seems independent of PPAR-α and without affecting mitochondrial function. Full article

(This article belongs to the Special Issue Molecular Research of Gastrointestinal Disease)

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15 pages, 3832 KiB

Open AccessArticle

Bone Marrow Stem Cells Derived from Nerves Have Neurogenic Properties and Potential Utility for Regenerative Therapy

by Leah C. Ott, Christopher Y. Han, Jessica L. Mueller, Ahmed A. Rahman, Ryo Hotta, Allan M. Goldstein and Rhian Stavely

Int. J. Mol. Sci. 2023, 24(6), 5211; https://doi.org/10.3390/ijms24065211 - 8 Mar 2023

Cited by 3 | Viewed by 2723

Abstract

Neurons and glia of the peripheral nervous system are derived from progenitor cell populations, originating from embryonic neural crest. The neural crest and vasculature are intimately associated during embryonic development and in the mature central nervous system, in which they form a neurovascular unit comprised of neurons, glia, pericytes, and vascular endothelial cells that play important roles in health and disease. Our group and others have previously reported that postnatal populations of stem cells originating from glia or Schwann cells possess neural stem cell qualities, including rapid proliferation and differentiation into mature glia and neurons. Bone marrow receives sensory and sympathetic innervation from the peripheral nervous system and is known to contain myelinating and unmyelinating Schwann cells. Herein, we describe a population of neural crest-derived Schwann cells residing in a neurovascular niche of bone marrow in association with nerve fibers. These Schwann cells can be isolated and expanded. They demonstrate plasticity in vitro, generating neural stem cells that exhibit neurogenic potential and form neural networks within the enteric nervous system in vivo following transplantation to the intestine. These cells represent a novel source of autologous neural stem cells for the treatment of neurointestinal disorders. Full article

(This article belongs to the Special Issue Molecular Research of Gastrointestinal Disease)

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25 pages, 4618 KiB

Open AccessArticle

Blocking Muscarinic Receptor 3 Attenuates Tumor Growth and Decreases Immunosuppressive and Cholinergic Markers in an Orthotopic Mouse Model of Colorectal Cancer

by Nyanbol Kuol, Majid Davidson, Jimsheena Karakkat, Rhiannon T. Filippone, Margaret Veale, Rodney Luwor, Sarah Fraser, Vasso Apostolopoulos and Kulmira Nurgali

Int. J. Mol. Sci. 2023, 24(1), 596; https://doi.org/10.3390/ijms24010596 - 29 Dec 2022

Cited by 14 | Viewed by 2925

Abstract

Tumor cells have evolved to express immunosuppressive molecules allowing their evasion from the host’s immune system. These molecules include programmed death ligands 1 and 2 (PD-L1 and PD-L2). Cancer cells can also produce acetylcholine (ACh), which plays a role in tumor development. Moreover, tumor innervation can stimulate vascularization leading to tumor growth and metastasis. The effects of atropine and muscarinic receptor 3 (M3R) blocker, 1,1-dimethyl-4-diphenylacetoxypiperidinium iodide (4-DAMP), on cancer growth and spread were evaluated in vitro using murine colon cancer cell line, CT-26, and in vivo in an orthotopic mouse model of colorectal cancer. In the in vitro model, atropine and 4-DAMP significantly inhibited CT-26 cell proliferation in a dose dependent manner and induced apoptosis. Atropine attenuated immunosuppressive markers and M3R via inhibition of EGFR/AKT/ERK signaling pathways. However, 4-DAMP showed no effect on the expression of PD-L1, PD-L2, and choline acetyltransferase (ChAT) on CT-26 cells but attenuated M3R by suppressing the phosphorylation of AKT and ERK. Blocking of M3R in vivo decreased tumor growth and expression of immunosuppressive, cholinergic, and angiogenic markers through inhibition of AKT and ERK, leading to an improved immune response against cancer. The expression of immunosuppressive and cholinergic markers may hold potential in determining prognosis and treatment regimens for colorectal cancer patients. This study’s results demonstrate that blocking M3R has pronounced antitumor effects via several mechanisms, including inhibition of immunosuppressive molecules, enhancement of antitumor immune response, and suppression of tumor angiogenesis via suppression of the AKT/ERK signaling pathway. These findings suggest a crosstalk between the cholinergic and immune systems during cancer development. In addition, the cholinergic system influences cancer evasion from the host’s immunity. Full article

(This article belongs to the Special Issue Molecular Research of Gastrointestinal Disease)

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Review

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14 pages, 1480 KiB

Open AccessReview

Programming Factors of Neonatal Intestinal Dysbiosis as a Cause of Disease

by Miljana Z. Jovandaric, Stefan Dugalic, Sandra Babic, Ivana R. Babovic, Srboljub Milicevic, Dejan Mihajlovic, Miljan Culjic, Tamara Zivanovic, Aleksandar Trklja, Bogdan Markovic, Vera Plesinac, Zorica Jestrovic, Biljana Medjo, Misela Raus and Miroslava Gojnic Dugalic

Int. J. Mol. Sci. 2023, 24(6), 5723; https://doi.org/10.3390/ijms24065723 - 17 Mar 2023

Cited by 5 | Viewed by 2590

Abstract

The intestinal microbiota consists of trillions of bacteria, viruses, and fungi that achieve a perfect symbiosis with the host. They perform immunological, metabolic, and endocrine functions in the body. The microbiota is formed intrauterine. Dysbiosis is a microbiome disorder characterized by an imbalance in the composition of the microbiota, as well as changes in their functional and metabolic activities. The causes of dysbiosis include improper nutrition in pregnant women, hormone therapy, the use of drugs, especially antibiotics, and a lack of exposure to the mother’s vaginal microbiota during natural birth. Changes in the intestinal microbiota are increasingly being identified in various diseases, starting in the early neonatal period into the adult period. Conclusions: In recent years, it has become more and more obvious that the components of the intestinal microbiota are crucial for the proper development of the immune system, and its disruption leads to disease. Full article

(This article belongs to the Special Issue Molecular Research of Gastrointestinal Disease)

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12 pages, 1386 KiB

Open AccessReview

Role of Ion Channels in the Chemotransduction and Mechanotransduction in Digestive Function and Feeding Behavior

by Zhenya Zhu, Yuhao Wu, Ziyu Liu, Yuezhou Li and Mizu Jiang

Int. J. Mol. Sci. 2022, 23(16), 9358; https://doi.org/10.3390/ijms23169358 - 19 Aug 2022

Cited by 6 | Viewed by 3386

Abstract

The gastrointestinal tract constantly communicates with the environment, receiving and processing a wide range of information. The contents of the gastrointestinal tract and the gastrointestinal tract generate mechanical and chemical signals, which are essential for regulating digestive function and feeding behavior. There are many receptors here that sense intestinal contents, including nutrients, microbes, hormones, and small molecule compounds. In signal transduction, ion channels are indispensable as an essential component that can generate intracellular ionic changes or electrical signals. Ion channels generate electrical activity in numerous neurons and, more importantly, alter the action of non-neurons simply and effectively, and also affect satiety, molecular secretion, intestinal secretion, and motility through mechanisms of peripheral sensation, signaling, and altered cellular function. In this review, we focus on the identity of ion channels in chemosensing and mechanosensing in the gastrointestinal tract. Full article

(This article belongs to the Special Issue Molecular Research of Gastrointestinal Disease)

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