scholarly journals The Roles of Dipeptidyl Peptidase 4 (DPP4) and DPP4 Inhibitors in Different Lung Diseases: New Evidence

2021 ◽  
Vol 12 ◽  
Author(s):  
Tianli Zhang ◽  
Xiang Tong ◽  
Shijie Zhang ◽  
Dongguang Wang ◽  
Lian Wang ◽  
...  
Keyword(s):  
Lung Diseases ◽  
Lung Parenchyma ◽  
Dipeptidyl Peptidase ◽  
Soluble Form ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Dipeptidyl Peptidase 4 ◽  
Dpp4 Inhibitors ◽  
Transmembrane Glycoprotein ◽  
Potential Biomarker

CD26/Dipeptidyl peptidase 4 (DPP4) is a type II transmembrane glycoprotein that is widely expressed in various organs and cells. It can also exist in body fluids in a soluble form. DPP4 participates in various physiological and pathological processes by regulating energy metabolism, inflammation, and immune function. DPP4 inhibitors have been approved by the Food and Drug Administration (FDA) for the treatment of type 2 diabetes mellitus. More evidence has shown the role of DPP4 in the pathogenesis of lung diseases, since it is highly expressed in the lung parenchyma and the surface of the epithelium, vascular endothelium, and fibroblasts of human bronchi. It is a potential biomarker and therapeutic target for various lung diseases. During the coronavirus disease-19 (COVID-19) global pandemic, DPP4 was found to be an important marker that may play a significant role in disease progression. Some clinical trials on DPP4 inhibitors in COVID-19 are ongoing. DPP4 also affects other infectious respiratory diseases such as Middle East respiratory syndrome and non-infectious lung diseases such as pulmonary fibrosis, lung cancer, chronic obstructive pulmonary disease (COPD), and asthma. This review aims to summarize the roles of DPP4 and its inhibitors in infectious lung diseases and non-infectious diseases to provide new insights for clinical physicians.

scholarly journals Protease-Specific Biomarkers to Analyse Protease Inhibitors for Emphysema Associated with Alpha 1-Antitrypsin Deficiency. An Overview of Current Approaches

2021 ◽  
Vol 22 (3) ◽  
pp. 1065
Author(s):  
Simona Viglio ◽  
Elisabeth G. Bak ◽  
Iris G. M. Schouten ◽  
Paolo Iadarola ◽  
Jan Stolk
Keyword(s):  
Serine Proteases ◽  
Lung Parenchyma ◽  
New Drugs ◽  
Chronic Obstructive ◽  
Augmentation Therapy ◽  
Lung Function Decline ◽  
Obstructive Pulmonary Disease ◽  
Antitrypsin Deficiency ◽  
Novel Biomarkers ◽  
Alpha1 Antitrypsin

As a known genetic cause of chronic obstructive pulmonary disease (COPD), alpha1-antitrypsin deficiency (AATD) can cause severe respiratory problems at a relatively young age. These problems are caused by decreased or absent levels of alpha1-antitrypsin (AAT), an antiprotease which is primarily functional in the respiratory system. If the levels of AAT fall below the protective threshold of 11 µM, the neutrophil-derived serine proteases neutrophil elastase (NE) and proteinase 3 (PR3), which are targets of AAT, are not sufficiently inhibited, resulting in excessive degradation of the lung parenchyma, increased inflammation, and increased susceptibility to infections. Because other therapies are still in the early phases of development, the only therapy currently available for AATD is AAT augmentation therapy. The controversy surrounding AAT augmentation therapy concerns its efficiency, as protection of lung function decline is not demonstrated, despite the treatment’s proven significant effect on lung density change in the long term. In this review article, novel biomarkers of NE and PR3 activity and their use to assess the efficacy of AAT augmentation therapy are discussed. Furthermore, a series of seven synthetic NE and PR3 inhibitors that can be used to evaluate the specificity of the novel biomarkers, and with potential as new drugs, are discussed.

scholarly journals Methylation of SERPINA1 gene promoter may predict chronic obstructive pulmonary disease in patients affected by acute coronary syndrome

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
John Charles Rotondo ◽  
Giorgio Aquila ◽  
Lucia Oton-Gonzalez ◽  
Rita Selvatici ◽  
Paola Rizzo ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Acute Coronary Syndrome ◽  
Pulmonary Disease ◽  
Blood Cells ◽  
Gene Promoter ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Coronary Syndrome ◽  
Copd Patients ◽  
Potential Biomarker

Abstract Background Diagnostic biomarkers for detecting chronic obstructive pulmonary disease (COPD) in acute coronary syndrome (ACS) patients are not available. SERPINA1, coding for the most potent circulating anti-inflammatory protein in the lung, has been found to be differentially methylated in blood cells from COPD patients. This study aimed to investigate the methylation profile of SERPINA1 in blood cells from ACS patients, with (COPD+) or without COPD (COPD−). Methods Blood samples were from 115 ACS patients, including 30 COPD+ and 85 COPD− according to lung function phenotype, obtained with spirometry. DNA treated with sodium bisulfite was PCR-amplified at SERPINA1 promoter region. Methylation analysis was carried out by sequencing the PCR products. Lymphocytes count in ACS patients was recorded at hospital admission and discharge. Results SERPINA1 was hypermethylated in 24/30 (80%) COPD+ and 48/85 (56.5%) COPD− (p < 0.05). Interestingly, at hospital discharge, lymphocytes count was higher in COPD− patients carrying SERPINA1 hypermethylated (1.98 × 103 ± 0.6 cell/µl) than in COPD− carrying SERPINA1 hypomethylated (1.7 × 103 ± 0.48 cell/µl) (p < 0.05). Conclusions SERPINA1 is hypermethylated in blood cells from COPD+ patients. COPD− carrying SERPINA1 hypermethylated and high lymphocytes count may be at risk of COPD development. Therefore, SERPINA1 hypermethylation may represent a potential biomarker for predicting COPD development in ACS patients.

scholarly journals The roles of exosomal miRNAs and lncRNAs in lung diseases

2019 ◽  
Vol 4 (1) ◽  
Author(s):  
Yang Li ◽  
Zhengrong Yin ◽  
Jinshuo Fan ◽  
Siyu Zhang ◽  
Weibing Yang
Keyword(s):  
Lung Cancer ◽  
Information Exchange ◽  
Lung Diseases ◽  
Cell Communication ◽  
Diagnostic Methods ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Diagnostic Biomarkers ◽  
Exosomal Mirnas ◽  
New Ideas

Abstract An increasing number of studies have reported that exosomes released from various cells can serve as mediators of information exchange between different cells. With further exploration of exosome content, a more accurate molecular mechanism involved in the process of cell-to-cell communication has been revealed; specifically, microRNAs (miRNAs) and long noncoding RNAs (lncRNAs) are shuttled by exosomes. In addition, exosomal miRNAs and lncRNAs may play vital roles in the pathogenesis of several respiratory diseases, such as chronic obstructive pulmonary disease (COPD), lung cancer, and asthma. Consequently, exosomal miRNAs and lncRNAs show promise as diagnostic biomarkers and therapeutic targets in several lung diseases. This review will summarize recent knowledge about the roles of exosomal miRNAs and lncRNAs in lung diseases, which has shed light on the discovery of novel diagnostic methods and treatments for these disorders. Because there is almost no published literature about exosomal lncRNAs in COPD, asthma, interstitial lung disease, or tuberculosis, we summarize the roles of exosomal lncRNAs only in lung cancer in the second section. This may inspire some new ideas for researchers who are interested in whether lncRNAs shuttled by exosomes may play roles in other lung diseases.

scholarly journals Cell therapy for lung disease

2017 ◽  
Vol 26 (144) ◽  
pp. 170044 ◽  
Author(s):  
Sabine Geiger ◽  
Daniela Hirsch ◽  
Felix G. Hermann
Keyword(s):  
Clinical Studies ◽  
Therapeutic Approach ◽  
Lung Diseases ◽  
Distress Syndrome ◽  
Treatment Options ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Cell Therapies ◽  
Promising Therapeutic Approach ◽  
Preclinical And Clinical Studies

Besides cancer and cardiovascular diseases, lung disorders are a leading cause of morbidity and death worldwide. For many disease conditions no effective and curative treatment options are available. Cell therapies offer a novel therapeutic approach due to their inherent anti-inflammatory and anti-fibrotic properties. Mesenchymal stem/stromal cells (MSC) are the most studied cell product. Numerous preclinical studies demonstrate an improvement of disease-associated parameters after MSC administration in several lung disorders, including chronic obstructive pulmonary disease, acute respiratory distress syndrome and idiopathic pulmonary fibrosis. Furthermore, results from clinical studies using MSCs for the treatment of various lung diseases indicate that MSC treatment in these patients is safe. In this review we summarise the results of preclinical and clinical studies that indicate that MSCs are a promising therapeutic approach for the treatment of lung diseases. Nevertheless, further investigations are required.

scholarly journals Angiotensin-Converting Enzyme 2 (ACE2) as a Potential Diagnostic and Prognostic Biomarker for Chronic Inflammatory Lung Diseases

Genes ◽  
2021 ◽  
Vol 12 (7) ◽  
pp. 1054
Author(s):  
Dejan Marčetić ◽  
Miroslav Samaržija ◽  
Andrea Vukić Dugac ◽  
Jelena Knežević
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Lung Diseases ◽  
Balance Control ◽  
Chronic Obstructive ◽  
Electrolyte Balance ◽  
Control Mechanisms ◽  
Pathophysiological Mechanism ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Potential Biomarker

Chronic inflammatory lung diseases are characterized by uncontrolled immune response in the airways as their main pathophysiological manifestation. The lack of specific diagnostic and therapeutic biomarkers for many pulmonary diseases represents a major challenge for pulmonologists. The majority of the currently approved therapeutic approaches are focused on achieving disease remission, although there is no guarantee of complete recovery. It is known that angiotensin-converting enzyme 2 (ACE2), an important counter-regulatory component of the renin–angiotensin–aldosterone system (RAAS), is expressed in the airways. It has been shown that ACE2 plays a role in systemic regulation of the cardiovascular and renal systems, lungs and liver by acting on blood pressure, electrolyte balance control mechanisms and inflammation. Its protective role in the lungs has also been presented, but the exact pathophysiological mechanism of action is still elusive. The aim of this study is to review and discuss recent findings about ACE2, including its potential role in the pathophysiology of chronic inflammatory lung diseases:, i.e., chronic obstructive pulmonary disease, asthma, and pulmonary hypertension. Additionally, in the light of the coronavirus 2019 disease (COVID-19), we will discuss the role of ACE2 in the pathophysiology of this disease, mainly represented by different grades of pulmonary problems. We believe that these insights will open up new perspectives for the future use of ACE2 as a potential biomarker for early diagnosis and monitoring of chronic inflammatory lung diseases.

scholarly journals Chronic Obstructive Pulmonary Disease: NHLBI Workshop on the Primary Prevention of Chronic Lung Diseases

2014 ◽  
Vol 11 (Supplement 3) ◽  
pp. S154-S160 ◽  
Author(s):  
M. Bradley Drummond ◽  
A. Sonia Buist ◽  
James D. Crapo ◽  
Robert A. Wise ◽  
Stephen I. Rennard
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Primary Prevention ◽  
Pulmonary Disease ◽  
Lung Diseases ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Chronic Lung Diseases

The state of the cardiovascular system in occupational bronchitis and chronic obstructive pulmonary disease, not associated with the impact of harmful industrial factors

2021 ◽  
pp. 55-68
Author(s):  
Vyacheslav S. Lotkov ◽  
Anton Vladimirovich Glazistov ◽  
Antonina G. Baykova ◽  
Marina Yuryevna Vostroknutova ◽  
Natalia E. Lavrentieva
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Cardiovascular System ◽  
Pulmonary Disease ◽  
Lung Diseases ◽  
Chronic Obstructive ◽  
External Respiration ◽  
Obstructive Pulmonary Disease ◽  
Occupational Lung Diseases ◽  
The Right ◽  
The Impact

The formation and progression of chronic dust bronchitis and chronic bronchitis of toxic-chemical etiology, chronic obstructive pulmonary disease is accompanied by an increase in the degree of ventilation disorders, echocardiographic signs of hypertrophy and dilatation of the right ventricle are formed, typical for chronic pulmonary heart disease. The progression of disturbances in the function of external respiration in dusty lung diseases leads to a decrease in myocardial contractility. The detection of hemodynamic disturbances at the early stages of the development of occupational lung diseases indicates the need for individual monitoring of the functional state of the cardiovascular system in the process of contact with industrial aerosols, especially in groups of workers with long-term exposure.

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