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• ↓ 3.7
• ↓ Advances in Understanding Calcium Sensitization in Gastrointestinal Smooth Muscles: Pathways, Interstitial Cells, and Disease
• ↓ Gastroesophageal Reflux Disease and Reflux-like Phenotypes: Using Lyon Consensus 2.0 to Guide Clinical Approach
• ↓ Confocal Laser Endomicroscopy With Duodenal Food Challenge Does Not Predict Triggering Food Items in Eosinophilic Esophagitis: Results From a Pilot Trial
• ↓ The Utility of the Functional Sphincter Area: A Novel Functional Lumen Imaging Probe Parameter for the Assessment of Anal Sphincter Structure and Function in Fecal Incontinence
• ↓ The Fermentable Oligosaccharides, Disaccharides, Monosaccharides, and Polyols Diet Is Effective in Irritable Bowel Syndrome With Constipation: A Single Center Tertiary Care Clinical Practice Evaluation
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"Schematic diagram of calcium sensitization pathways in smooth muscle cells (SMCs). Depolarization of the SMC plasma membrane opens dihydropyridine-sensitive voltage-dependent Ca2+ channels (VDCC), increasing the concentration of Ca2+ in the cytoplasm. Ca2+ binds to calmodulin (CaM), which binds to and activates myosin light chain kinase (MLCK), which phosphorylates the regulatory light chain of thick filament myosin to enable myosin binding to thin filament actin for cross-bridge cycling and muscle contraction. Simultaneously, voltage-dependent Ca2+ influx activates protein kinase C (PKC), which phosphorylates protein phosphatase 1 regulatory subunit 14A (CPI-17). Phosphorylated CPI-17 binds to and inhibits myosin light chain phosphatase (MLCP), inhibiting the dephosphorylation of myosin regulatory light chain. Thus, during voltage-dependent Ca2+ influx, the ratio of MLCK activity to MLCP activity is higher and contraction is augmented because the PKC-mediated calcium sensitization pathway is activated. In receptor-mediated smooth muscle contraction, cholinergic agonists bind to the muscarinic M3 receptor and activate Gq12/13. Gq12/13 stimulates guanosine 5′-triphosphate (GTP) binding to RhoA, which binds to and activates Rho-associated coiled-coil kinase (ROCK). ROCK phosphorylates myosin phosphatase targeting subunit 1 (MYPT1), and other proteins, leading to reduced MLCP activity. Gq12/13 also activates phospholipase Cβ (PLCβ), generating inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3 releases Ca2+ from intracellular stores into the cytoplasm. This Ca2+ binds to CaM which activates MLCK to phosphorylate and enable myosin to bind to thin filament actin for cross-bridge cycling. Ca2+ and DAG also bind to and activate PKC, which phosphorylates CPI-17 to further inhibit MLCP. Thus, during receptor-mediated contraction, the ratio of MLCK activity to MLCP activity is even higher, and contraction is further augmented because both the PKC- and ROCK-mediated calcium sensitization pathways are activated. CCh, carbachol; PP1cβ, catalytic type 1 phosphatase subunit; M20, 20 kDa regulatory subunit of MLCP."

"Interrelationships between Montreal Consensus, Lyon Consensus 2.0 and Rome Criteria. Montreal Consensus starts with patients with troublesome symptoms, but only a third of these patients will have the mucosal injury phenotype. Lyon Consensus 2.0 adapted findings of esophageal mucosal injury into conclusive evidence for gastroesophageal reflux disease (GERD) and defined the abnormal reflux burden phenotype. Rome Criteria, on the other hand, requires exclusion of both mucosal injury and abnormal reflux burden phenotypes to identify pure disorders of gut brain interaction (DGBI), and the updated version utilizes Lyon Consensus 2.0 criteria for this purpose. Hypervigilance and symptom-specific anxiety can be present in all the symptom phenotypes, and DGBI can overlap with conclusive GERD diagnosed using Lyon Consensus 2.0 criteria. The ultimate goal is symptom relief, achieved primary through management of GERD in the mucosal injury and abnormal reflux burden phenotypes, and through management of DGBI when evidence of GERD is not found."

Key Topics & Focus Areas for jnmjournal.org:

3.7

Advances in Understanding Calcium Sensitization in Gastrointestinal Smooth Muscles: Pathways, Interstitial Cells, and Disease

Gastroesophageal Reflux Disease and Reflux-like Phenotypes: Using Lyon Consensus 2.0 to Guide Clinical Approach

Confocal Laser Endomicroscopy With Duodenal Food Challenge Does Not Predict Triggering Food Items in Eosinophilic Esophagitis: Results From a Pilot Trial

The Utility of the Functional Sphincter Area: A Novel Functional Lumen Imaging Probe Parameter for the Assessment of Anal Sphincter Structure and Function in Fecal Incontinence

The Fermentable Oligosaccharides, Disaccharides, Monosaccharides, and Polyols Diet Is Effective in Irritable Bowel Syndrome With Constipation: A Single Center Tertiary Care Clinical Practice Evaluation