Introduction

ESC CardioMed ◽  
2018 ◽  
pp. 1081-1082
Author(s):  
Gerhard Rogler
Keyword(s):  
Heart Failure ◽  
Heart Disease ◽  
Chronic Heart Failure ◽  
Bacterial Translocation ◽  
Gastrointestinal Disease ◽  
Intestinal Barrier ◽  
Mucosal Barrier ◽  
Intestinal Barrier Function ◽  
Oral Drug ◽  
Intestinal Microcirculation

Gastrointestinal disease and heart disease seem to be two groups of diseases that do not have much in common. However, recent insights have changed this assumption: the intestine’s basic functions, digestion and absorption, are obviously clinically relevant for almost all oral drug treatments of diseases. An impairment of intestinal barrier function is followed by increased bacterial translocation across the intestinal mucosa leading to increased levels of circulating bacteria and bacterial products. This is assumed to be associated with atherosclerosis and chronic heart failure. Vice versa, an impaired cardiac function in the setting of chronic heart failure may lead to a defect in the mucosal barrier and increased bacterial translocation via changes in intestinal microcirculation. In addition, recent evidence indicates that conditions such as metabolic syndrome or obesity—certainly risk factors for heart disease—are influenced by intestinal microbiota composition.

Introduction

ESC CardioMed ◽  
2018 ◽  
pp. 1081-1082
Author(s):  
Gerhard Rogler
Keyword(s):  
Heart Failure ◽  
Heart Disease ◽  
Chronic Heart Failure ◽  
Bacterial Translocation ◽  
Gastrointestinal Disease ◽  
Intestinal Barrier ◽  
Mucosal Barrier ◽  
Intestinal Barrier Function ◽  
Oral Drug ◽  
Intestinal Microcirculation

Gastrointestinal disease and heart disease seem to be two groups of diseases that do not have much in common. However, recent insights have changed this assumption: the intestine’s basic functions, digestion and absorption, are obviously clinically relevant for almost all oral drug treatments of diseases. An impairment of intestinal barrier function is followed by increased bacterial translocation across the intestinal mucosa leading to increased levels of circulating bacteria and bacterial products. This is assumed to be associated with atherosclerosis and chronic heart failure. Vice versa, an impaired cardiac function in the setting of chronic heart failure may lead to a defect in the mucosal barrier and increased bacterial translocation via changes in intestinal microcirculation. In addition, recent evidence indicates that conditions such as metabolic syndrome or obesity—certainly risk factors for heart disease—are influenced by intestinal microbiota composition.

MicroRNA Determines the Fate of Intestinal Epithelial Cell Differentiation and Regulates Intestinal Diseases

2019 ◽  
Vol 20 (7) ◽  
pp. 666-673 ◽  
Author(s):  
Sujuan Ding ◽  
Gang Liu ◽  
Hongmei Jiang ◽  
Jun Fang
Keyword(s):  
Target Genes ◽  
Gastrointestinal Disease ◽  
Intestinal Barrier ◽  
Vital Role ◽  
Intestinal Barrier Function ◽  
Intestinal Epithelial ◽  
Intestinal Function ◽  
Cell Fates ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation

The rapid self-renewal of intestinal epithelial cells enhances intestinal function, promotes the nutritional needs of animals and strengthens intestinal barrier function to resist the invasion of foreign pathogens. MicroRNAs (miRNAs) are a class of short-chain, non-coding RNAs that regulate stem cell proliferation and differentiation by down-regulating hundreds of conserved target genes after transcription via seed pairing to the 3' untranslated regions. Numerous studies have shown that miRNAs can improve intestinal function by participating in the proliferation and differentiation of different cell populations in the intestine. In addition, miRNAs also contribute to disease regulation and therefore not only play a vital role in the gastrointestinal disease management but also act as blood or tissue biomarkers of disease. As changes to the levels of miRNAs can change cell fates, miRNA-mediated gene regulation can be used to update therapeutic strategies and approaches to disease treatment.

scholarly journals The DNA Sensor AIM2 Protects against Streptozotocin-Induced Type 1 Diabetes by Regulating Intestinal Homeostasis via the IL-18 Pathway

Cells ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 959 ◽  
Author(s):  
Jefferson Antônio Leite ◽  
Gabriela Pessenda ◽  
Isabel C. Guerra-Gomes ◽  
Alynne Karen Mendonça de Santana ◽  
Camila André Pereira ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Gut Microbiota ◽  
Bacterial Translocation ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Dna Sensor ◽  
Proinflammatory Response

Pattern recognition receptors (PRRs), such as Nod2, Nlrp3, Tlr2, Trl4, and Tlr9, are directly involved in type 1 diabetes (T1D) susceptibility. However, the role of the cytosolic DNA sensor, AIM2, in T1D pathogenesis is still unknown. Here, we demonstrate that C57BL/6 mice lacking AIM2 (AIM2−/−) are prone to streptozotocin (STZ)-induced T1D, compared to WT C57BL/6 mice. The AIM2−/− mice phenotype is associated with a greater proinflammatory response in pancreatic tissues, alterations in gut microbiota and bacterial translocation to pancreatic lymph nodes (PLNs). These alterations are related to an increased intestinal permeability mediated by tight-junction disruption. Notably, AIM2−/− mice treated with broad-spectrum antibiotics (ABX) are protected from STZ-induced T1D and display a lower pancreatic proinflammatory response. Mechanistically, the AIM2 inflammasome is activated in vivo, leading to an IL-18 release in the ileum at 15 days after an STZ injection. IL-18 favors RegIIIγ production, thus mitigating gut microbiota alterations and reinforcing the intestinal barrier function. Together, our findings show a regulatory role of AIM2, mediated by IL-18, in shaping gut microbiota and reducing bacterial translocation and proinflammatory response against insulin-producing β cells, which ultimately results in protection against T1D onset in an STZ-induced diabetes model.

scholarly journals New score scale for assessing the risk of establishing chronic heart failure with preserved ejection fraction

2021 ◽  
Vol 25 (3) ◽  
pp. 83-96
Author(s):  
O. M. Zherko ◽  
E. I. Shkrebneva
Keyword(s):  
Heart Failure ◽  
Heart Disease ◽  
Chronic Heart Failure ◽  
Ejection Fraction ◽  
Sinus Rhythm ◽  
Preserved Ejection Fraction ◽  
Dispersion Index ◽  
Diagnostic Reliability ◽  
Mechanical Dispersion ◽  
Instrumental Study

The aim of the study was to develop a score scale for assessing the high risk of establishing chronic heart failure with preserved ejection fraction (HFpEF), based on echocardiography (EchoCG) evidence.Materials and methods. A clinical and instrumental study of 175 patients, of which 108 (61.7%) women and 67 (38.3%) men, aged 71 [64; 78] years was performed in the 1st City Clinical Hospital in Minsk in 2017–2018. In order to validate the score scale for assessing the risk of HFpEF establishment in 2019–2020 a reproductive clinical and instrumental study of 129 patients was performed at the Minsk Scientific and Practical Center for Surgery, Transplantology and Hematology, of which 55 (42.6%) were men and 74 (57.4%) women aged 65 [58; 70] years. Inclusion criteria: sinus rhythm, essential arterial hypertension, chronic coronary heart disease: atherosclerotic heart disease, past myocardial infarction of left ventricle (LV), after which at least six months have passed, necessary to stabilize the structural and functional parameters of the LV, HFpEF, informed consent of the patient. Exclusion criteria: primary mitral regurgitation, mitral stenosis, mitral valve repair or prosthetics, congenital heart defects, acute and chronic diseases of the kidneys, lungs. EchoCG was performed on ultrasound machines Siemens Acuson S1000 (Germany) and Vivid E9 (GE Healthcare, USA).Results. The developed scale for assessing the risk of establishing HFpEF in a patient with sinus rhythm including the criteria: LV diastolic dysfunction type II – 47 points, deceleration time of peak E of the transmitral blood flow DTE ≤171 ms – 25 points, the speed of early diastolic movement of the septal part of the mitral fibrous ring e'septal ≤7 cm/s – 25 points, LV early diastolic filling index E/е'septal >7.72 – 20 points, index of the end-systolic volume of the left atrium >34.3 ml/m2 – 24 points, has high diagnostic reliability (AUC 0.96, sensitivity (S) 96.6%, specificity (Sp) 83.2%) and reproducibility of results in an examination cohort of patients (AUC 0.99, S 98.8%, Sp 98.0%). A total score > 45 indicates a high probability of HFpEF. If the total score is ≤45, it is recommended to perform 2D Speckle Tracking EchoCG. The leading patho-functional mechanisms for the development of HFpEF are a decrease of LV global systolic longitudinal strain GLSAVG > −18.9% (S 94.9%, Sp 98.0%), GLS of the right ventricle (RV) > −19.9% (S 76.5%, Sp 88.5%), mechanical dispersion with LV mechanical dispersion index > 54.69 ms (S 70.7%, Sp 90.2%), RV mechanical dispersion index > 50.29 msec (S 78.1%, Sp 73.9%) and ventricular dyssynergy with LV global post systolic index >5.59% (S 82.6%, Sp 87.5%), RV global post systolic index > 2.17% (S 84.5%, Sp 69.9%).Conclusions. The use of the developed scale will improve the efficiency of ultrasound imaging of HFpEF.

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