Aortic stiffness and polymorphisms of collagen-1 type 1a gene in COPD patients

Brodskaya, T. A.; Невзорова, В. А.; Захарчук, Н. В.; Repina, N. I.

doi:10.15406/jlprr.2018.05.00167

Cited by 3 publications

(4 citation statements)

References 25 publications

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“…In particular, endothelium activation is an important factor of initiation, development and persistence of inflammation, and vessel and tissue remodeling, in particular emphysema. It is not by chance that the relationship of emphysema of the lungs is described in violation of the mechanical properties of the aorta and excessive stiffness of other exponents' bloodstream [4,6,64]. At the basis of these pathological processes are common (genetically determined and pathologically determined) mechanisms associated with impaired collagen-elastin metabolism.…”

Section: Discussionmentioning

confidence: 99%

Smoking and COPD: Endothelium-Related and Neuro-mediated Emphysema Mechanisms

Невзорова¹,

Brodskaya²,

Гилифанов³

2020

Update in Respiratory Diseases

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This chapter describes endothelium-related and neuro-mediated mechanisms of emphysema development in chronic obstructive pulmonary disease (COPD) and smoking on the basis of previously completed studies, literature data, and own researches. As components of neurogenic inflammation in the processes of tissue remodeling in emphysema, we describe the distribution and activity of the substance P, neurokinin-1 and its receptor, tissue metalloproteinases and their tissue inhibitors in the lungs during the entire experimental period, the modeling of COPD in rats with a smoking model. We also analyzed the content of neurokinin system markers, the localization, and markers of tissue metalloproteinases in human lung tissue structures. We have confidence that there is a special morphofunctional continuum of development of lower respiratory tract remodeling in response to chronic exposure to tobacco smoke and the development of inflammation in COPD. New data suggest that imbalance of neuro-mediated interactions, alteration of vasomotoric signaling mechanisms, secretion, mucociliary clearance, cytoprotection involving substance P-dependent components with impaired content, and development of dystopia of matrix metalloproteinases and their tissue inhibitors are involved in the initiation of morphological restructuring. Research in this direction should be continued to allow approaches to the development of preventive and therapeutic strategies for emphysema.

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Section: Discussionmentioning

confidence: 99%

Smoking and COPD: Endothelium-Related and Neuro-mediated Emphysema Mechanisms

Невзорова¹,

Brodskaya²,

Гилифанов³

2020

Update in Respiratory Diseases

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“…Collagen type I, is an essential component of the extracellular matrix (ECM) in blood vessels, providing mechanical strength and contractility [35]. An increase in collagen type I is associated with arterial stiffness [36]. TGF-α, is a member of the epidermal growth factor (EGF) family that plays a role in cell proliferation, differentiation, and migration [37].…”

Section: Plos Onementioning

confidence: 99%

Proteomic analysis of pulmonary arteries and lung tissues from dogs affected with pulmonary hypertension secondary to degenerative mitral valve disease

Sakarin,

Rungsipipat,

Roytrakul

et al. 2024

PLoS ONE

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In dogs with degenerative mitral valve disease (DMVD), pulmonary hypertension (PH) is a common complication characterized by abnormally elevated pulmonary arterial pressure (PAP). Pulmonary arterial remodeling is the histopathological changes of pulmonary artery that has been recognized in PH. The underlying mechanisms that cause this arterial remodeling are poorly understood. This study aimed to perform shotgun proteomics to investigate changes in protein expression in pulmonary arteries and lung tissues of DMVD dogs with PH compared to normal control dogs and DMVD dogs without PH. Tissue samples were collected from the carcasses of 22 small-sized breed dogs and divided into three groups: control (n = 7), DMVD (n = 7) and DMVD+PH groups (n = 8). Differentially expressed proteins were identified, and top three upregulated and downregulated proteins in the pulmonary arteries of DMVD dogs with PH including SIK family kinase 3 (SIK3), Collagen type I alpha 1 chain (COL1A1), Transforming growth factor alpha (TGF-α), Apoptosis associated tyrosine kinase (AATYK), Hepatocyte growth factor activator (HGFA) and Tyrosine-protein phosphatase non-receptor type 13 (PTPN13) were chosen. Results showed that some of the identified proteins may play a role in the pathogenesis of pulmonary arterial remodeling. This study concluded shotgun proteomics has potential as a tool for exploring candidate proteins associated with the pathogenesis of PH secondary to DMVD in dogs.

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“…В свою очередь, окисленные липопротеины в интиме сосудистой стенки, выполняя функцию аттрактантов для хемотаксиса лейкоцитов и моноцитов, позволяют запустить неконтролируемый воспалительный каскад с участием широкого спектра провоспалительных цитокинов. Итогом последнего является системный воспалительный ответ с нарушением функции и изменением архитектоники сосудистой стенки, последствиями которой является избыточная жесткость или необратимая атеросклеротическая деструкция [20,21,26]. Хроническое воздействие табачного дыма и продуктов сгорания табака приводит к хронической системной воспалительной реакции, окислительному стрессу, эндотелиальной дисфункции и вызывает морфофункциональное повреждение иных органов-мишеней.…”

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“…Итак, результаты исследований с участием людей и животных показывают, что сосудистый эндотелий инициирует и модулирует основные патоморфологические процессы при ХОБЛ и курении, в том числе является важным фактором инициации, развития и персистенции воспаления и ремоделирования сосудов и тканей, включая поражение МДП с развитием деструкции легочной ткани и эмфиземы. Поэтому неслучайно эмфизема легких описывается во взаимосвязи с нарушением механических свойств аорты и ремоделирования сосудистого русла на всем протяжении [4,9,20,26]. В основе этих патологических процессов лежат общие (генетически и патологически детерминированные) механизмы, связанные с воспалением и нарушением коллаген-эластинового обмена.…”

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Endothelium-related and neuro-mediated mechanisms of emphysema development in chronic obstructive pulmonary disease

Brodskaya

Невзорова

Vasileva

et al. 2020

Terapevticheskii arkhiv

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Emphysema is one of the main manifestations of chronic obstructive pulmonary disease (COPD), and smoking is one of the most significant risk factors. The results of studies in humans and animals show the vascular endothelium initiates and modulates the main pathological processes in COPD and smoking is an important factor initiating, developing and persisting inflammation and remodeling of blood vessels and tissues, including the destruction of small respiratory tracts with the development of lung tissue destruction and emphysema. The latest studies describe mechanisms not just associated with the endothelium, but specific neuro-mediated mechanisms. There is reason to believe that neuro-mediated and neuro-similar mechanisms associated and not related to endothelial dysfunction may play the significant role in the pathogenesis of COPD and emphysema formation. Information about components and mechanisms of neurogenic inflammation in emphysema development is fragmentary and not systematized in the literature. It is described that long-term tobacco smoking can initiate processes not only of cells and tissues damage, but also become a trigger for excessive release of neurotransmitters, which entails whole cascades of adverse reactions that have an effect on emphysema formation. With prolonged and/or intensive stimulation of sensor fibers, excessive release of neuropeptides is accompanied by a number of plastic and destructive processes due to a cascade of pathological reactions of neurogenic inflammation, the main participants of which are classical neuropeptides and their receptors. The most important consequences can be the maintenance and stagnation of chronic inflammation, activation of the mechanisms of destruction and remodeling, inadequate repair processes in response to damage, resulting in irreversible loss of lung tissue. For future research, there is interest to evaluate the possibilities of therapeutic and prophylactic effects on neuro-mediated mechanisms of endothelial dysfunction and damage emphysema in COPD and smoking development.

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Aortic stiffness and polymorphisms of collagen-1 type 1a gene in COPD patients

Cited by 3 publications

References 25 publications

Smoking and COPD: Endothelium-Related and Neuro-mediated Emphysema Mechanisms

Smoking and COPD: Endothelium-Related and Neuro-mediated Emphysema Mechanisms

Proteomic analysis of pulmonary arteries and lung tissues from dogs affected with pulmonary hypertension secondary to degenerative mitral valve disease

Endothelium-related and neuro-mediated mechanisms of emphysema development in chronic obstructive pulmonary disease

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