Lipid Peroxidation in Patients With Copd and Chronic Heart Failure.

Klimanov, Igor; Khaletskaya, А.I.; Kuznechov, A.N.; Kontorschikova, Klavdia; Kubysheva, Nailya; Leonova, Daria; Bobkova, A S; Soodaeva, Svetlana

doi:10.1183/13993003.congress-2018.pa931

Cited by 1 publication

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“…ROS directly damage biological molecules and lung extracellular matrix, leading to cell dysfunction or death, and activate NF-κB, which enhances the expression of inflammatory genes such as IL-8 and TNF-α, important in COPD, contributing to reversible airway narrowing [176]. Neutrophils show increased oxide anion (O 2 − ) levels [177], and lipid peroxidation products such as thiobarbituric acid (TBA), linoleic acid (LA), and F2-isoprostane are also increased [178]. Conversely, the plasma antioxidant capacity is decreased [179].…”

Section: Chronic Obstructive Pulmonary Disease (Copd)mentioning

confidence: 99%

Airway Redox Homeostasis and Inflammation Gone Awry: From Molecular Pathogenesis to Emerging Therapeutics in Respiratory Pathology

Checa

Aran

2020

IJMS

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As aerobic organisms, we are continuously and throughout our lifetime subjected to an oxidizing atmosphere and, most often, to environmental threats. The lung is the internal organ most highly exposed to this milieu. Therefore, it has evolved to confront both oxidative stress induced by reactive oxygen species (ROS) and a variety of pollutants, pathogens, and allergens that promote inflammation and can harm the airways to different degrees. Indeed, an excess of ROS, generated intrinsically or from external sources, can imprint direct damage to key structural cell components (nucleic acids, sugars, lipids, and proteins) and indirectly perturb ROS-mediated signaling in lung epithelia, impairing its homeostasis. These early events complemented with efficient recognition of pathogen- or damage-associated recognition patterns by the airway resident cells alert the immune system, which mounts an inflammatory response to remove the hazards, including collateral dead cells and cellular debris, in an attempt to return to homeostatic conditions. Thus, any major or chronic dysregulation of the redox balance, the air–liquid interface, or defects in epithelial proteins impairing mucociliary clearance or other defense systems may lead to airway damage. Here, we review our understanding of the key role of oxidative stress and inflammation in respiratory pathology, and extensively report current and future trends in antioxidant and anti-inflammatory treatments focusing on the following major acute and chronic lung diseases: acute lung injury/respiratory distress syndrome, asthma, chronic obstructive pulmonary disease, pulmonary fibrosis, and cystic fibrosis.

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Section: Chronic Obstructive Pulmonary Disease (Copd)mentioning

confidence: 99%