Smoking, Respiratory Diseases and Endothelial Dysfunction

Невзорова, В. А.; Brodskaya, T. A.; Захарчук, Н. В.

doi:10.5772/intechopen.73555

Cited by 5 publications

(14 citation statements)

References 57 publications

(87 reference statements)

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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%

“…All disorders begin with local and systemic inflammation, hypoxia and oxidative stress, and lead to an imbalance of proteases-antiproteases, loss of recovery and destruction of lung tissue. Activation and dysfunction of the endothelium involves, first of all, imbalance of the endothelium and its associated mechanisms, which Smoking and COPD: Endothelium-Related and Neuro-mediated Emphysema Mechanisms DOI: http://dx.doi.org /10.5772/intechopen.85927 are due to the following disorders in the pathogenesis of COPD [4]. Separately, we would like to pay attention on some endothelium-dependent factors.…”

Section: Endothelium-related and Neuro-mediated Mechanisms Of Emphysementioning

confidence: 99%

“…It is known that tobacco smoke is a powerful inducer of the destruction of the respiratory epithelium throughout, followed by its morphofunctional remodeling [4,31,32]. Initiation of cell and tissue injury processes in prolonged exposure to smoking can take place due to excess release of neurotransmitters from sensitive afferent nerve fibers of the nervous vagus system.…”

Section: Endothelium-related and Neuro-mediated Mechanisms Of Emphysementioning

confidence: 99%

“…In GOLD 2018, COPD was defined as a common, preventable, and treatable disease that is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases [1]. It was mentioned that chronic respiratory symptoms also exist in individuals with normal spirometry and a significant number of smokers without airflow limitation have structural evidence of lung disease manifested by the varying presence of emphysema, airway wall thickening, and gas trapping [2][3][4]. Really, smoking is a major risk factor for COPD, and it plays an important role in lung tissue destruction development.…”

Section: Introductionmentioning

confidence: 99%

“…can cause direct damage to endothelial cells due to expression of adhesion molecules on their surface and intensification of lipid peroxidation [2,[5][6][7]. But the main underlying cause of structural changes is chronic inflammation, which is confirmed by numerous studies [1,[4][5][6]. Even in mild COPD, or in smokers susceptible to emphysema [7,8], there are significant abnormalities in pulmonary microvascular blood flow that worsen with disease progression [9].…”

Section: Introductionmentioning

confidence: 99%

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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%

Section: Endothelium-related and Neuro-mediated Mechanisms Of Emphysementioning

confidence: 99%

Section: Endothelium-related and Neuro-mediated Mechanisms Of Emphysementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Невзорова¹,

Brodskaya²,

Гилифанов³

2020

Update in Respiratory Diseases

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Impact of smoking on resin bonded restorations: A narrative review

Alonazi

2024

Tob. Induc. Dis.

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INTRODUCTION Smoking is a common risk factor for multiple diseases, including diabetes mellitus, cardiovascular diseases, pulmonary diseases, and different cancers. It is an established cause of multiple oral health conditions, in addition to adversely impairing the appearance of oral tissues. Smoking has also been identified to impact dental restorations' functional and esthetic aspects. This narrative review is focused on the significance of the esthetic consequences of smoking on resin-based dental restoration. It provides an understanding of the challenges dental professionals and patients face. METHODS A literature search was conducted to identify studies on the impact of smoking exposure on the esthetic appearance of composite restorations. The inclusion criteria were met by five studies selected for analysis. RESULTSThe studies revealed that conventional cigarettes cause more noticeable color changes than electronic cigarettes. Additionally, the choice of composite material significantly influences the color stability of dental restorations. Exposure to both smoking and staining agents could worsen the color alterations in dental restorations. Smokers may benefit from dental ceramics, which offer better aesthetics. Quantitative insights into these effects can be gained by incorporating delta E (ΔE) values and fluorescence intensity in esthetic evaluations. CONCLUSIONS The studies provide valuable insights into the multiple factors that can impact the aesthetics of dental restorations. Dental professionals should take into account the smoking type, composite material, and patient habits when planning treatments. Utilizing ΔE values and fluorescence intensity in esthetic evaluations can provide a more comprehensive understanding. Future research should focus on longitudinal studies, alternative materials, and individual patient profiles.

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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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Smoking, Respiratory Diseases and Endothelial Dysfunction

Cited by 5 publications

References 57 publications

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

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

Impact of smoking on resin bonded restorations: A narrative review

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

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