Medicina de Familia SEMERGEN, Год журнала: 2024, Номер 50(6), С. 102193 - 102193
Опубликована: Март 13, 2024
Язык: Английский
Medicina de Familia SEMERGEN, Год журнала: 2024, Номер 50(6), С. 102193 - 102193
Опубликована: Март 13, 2024
Язык: Английский
International Journal of Dermatology, Год журнала: 2025, Номер unknown
Опубликована: Март 22, 2025
Atopic dermatitis, prurigo nodularis, and chronic spontaneous urticaria are immune-mediated, inflammatory skin conditions characterized by intense itch disease-specific lesions. Despite their different clinical presentations, the three diseases unified an aberrant type 2 immune response involving cytokines, cells, sensory nerves that may underlie shared manifestations of inflammation pruritus. The nature these is associated with significant impairment in patients' quality life psychological disorders, such as anxiety depression. This article reviews its role atopic urticaria, focusing on pathophysiologic drivers each dermatologic condition. Understanding mechanisms seemingly distinct other concomitant critical for applying therapeutic interventions targeting pathway.
Язык: Английский
Процитировано
2Expert Opinion on Investigational Drugs, Год журнала: 2023, Номер 32(9), С. 793 - 802
Опубликована: Сен. 2, 2023
Introduction Excessive activity of neutrophil elastase (NE), the main enzyme present in azurophil granules cytoplasm, may cause tissue injury and remodeling various lung diseases, including acute (ALI)/acute respiratory distress syndrome (ARDS), which it is crucial to immune response inflammatory process. Consequently, NE a possible target for therapeutic intervention ALI/ARDS.
Язык: Английский
Процитировано
14Phytomedicine, Год журнала: 2024, Номер 126, С. 155273 - 155273
Опубликована: Янв. 6, 2024
Язык: Английский
Процитировано
6ERJ Open Research, Год журнала: 2024, Номер 10(5), С. 00177 - 2024
Опубликована: Май 9, 2024
Inflammation drives COPD pathogenesis and exacerbations. Although the conceptual framework major players in inflammatory milieu of have been long established, nuances cellular interactions etiological differences that create heterogeneity profiles treatment response continue to be revealed. This wealth data understanding is not only a boon researcher but also provides guidance clinician, moving field closer precision medicine. It through this lens review seeks describe processes at play COPD, relating inflammation pathological functional changes, identifying patient-specific disease-related factors may influence clinical observations, providing current insights on existing emerging anti-inflammatory treatments targets, including biological therapies phosphodiesterase (PDE) inhibitors.
Язык: Английский
Процитировано
5Drugs, Год журнала: 2024, Номер 84(9), С. 1157 - 1163
Опубликована: Авг. 28, 2024
Язык: Английский
Процитировано
5Nature Aging, Год журнала: 2024, Номер unknown
Опубликована: Ноя. 15, 2024
Chronic obstructive pulmonary disease (COPD) is a progressive, incurable associated with smoking and advanced age, ranking as the third leading cause of death worldwide. DNA damage loss central metabolite nicotinamide adenine dinucleotide (NAD+) may contribute to both aging COPD, presenting potential avenue for interventions. In this randomized, double-blind, placebo-controlled clinical trial, we treated patients stable COPD (n = 40) NAD+ precursor riboside (NR) 6 weeks followed-up 12 later. The primary outcome was change in sputum interleukin-8 (IL-8) from baseline week 6. estimated treatment difference between NR placebo IL-8 after −52.6% (95% confidence interval (CI): −75.7% −7.6%; P 0.030). This effect persisted until follow-up end (−63.7%: 95% CI −85.7% −7.8%; 0.034). For secondary outcomes, increased levels by more than twofold whole blood, whereas IL-6 plasma remained unchanged. exploratory analyses, showed indications upregulated gene pathways related genomic integrity airways reduced epigenetic aging, possibly through reduction cellular senescence. These analyses need be confirmed future trials. ClinicalTrials.gov identifier: NCT04990869 . Drivers physiological are also linked etiology chronic (COPD), including inflammation senescence, influenced metabolism. Norheim et al. performed randomized controlled trial testing whether boosting reduces airway inflammation.
Язык: Английский
Процитировано
4Expert Opinion on Drug Safety, Год журнала: 2024, Номер 23(7), С. 833 - 844
Опубликована: Май 30, 2024
Introduction The safety of β2-AR antagonists in the treatment patients with COPD continues to be a topic research and discussion within medical community. Emerging evidence suggests potentially benefits management this complex respiratory condition. However, display minimal preference for over β1-AR present therapeutic challenge management, necessitating an understanding small differences their pharmacological profiles clinical implications.
Язык: Английский
Процитировано
3CrystEngComm, Год журнала: 2024, Номер 26(28), С. 3783 - 3790
Опубликована: Янв. 1, 2024
Ensifentrine is a bifunctional dual phosphodiesterase 3/4 inhibitor with both anti-inflammatory and bronchodilatory properties. This research consists of three polymorph preparations ENSE their solubility chemical stability studies.
Язык: Английский
Процитировано
3Cell Biology International, Год журнала: 2024, Номер unknown
Опубликована: Окт. 4, 2024
Abstract Chronic obstructive pulmonary disease (COPD) is a pervasive and incapacitating respiratory condition, distinguished by airway inflammation the remodeling of lower tract. Central to its pathogenesis an intricate inflammatory process, wherein macrophages exert significant regulatory functions, High mobility group box 1 (HMGB1) emerges as pivotal mediator potentially driving COPD progression. This study explores hypothesis that HMGB1, within macrophages, modulates through mechanisms, focusing on influence macrophage polarization. Our investigation uncovered HMGB1 upregulated in context COPD, associated with enhanced proinflammatory M1 polarization induced cigarette smoke. linked suppressed cell proliferation apoptosis, indicative HMGB1's role disease's trajectory. The further implicates activation Nuclear factor kappa‐B (NF‐κB) signaling pathway chemokine which are likely amplify response characteristic COPD. findings underscore critical involvement pathogenesis, presenting it target for therapeutic intervention aimed at modulating inflammation.
Язык: Английский
Процитировано
3International Journal of COPD, Год журнала: 2024, Номер Volume 19, С. 2481 - 2495
Опубликована: Ноя. 1, 2024
Chronic obstructive pulmonary disease (COPD) is a progressive inflammatory condition often complicated by cardiovascular (CVD) due to shared pathways. This review explores the impacts of emerging anti-inflammatory therapies in COPD. Phosphodiesterase (PDE) inhibitors may offer effects with improved lung function but pose potential risks for arrhythmias when PDE3 inhibited although PDE4 reduce events improving endothelial and reducing thrombosis. Similarly, p38 mitogen-activated protein kinase (MAPK) phosphoinositide 3-kinase (PI3K) target COPD-related inflammation benefit COPD patients CVD. MAPK cardiac fibrosis, enhance contractility lower risk arrhythmia. PI3K PI3K/Akt pathway, which drives atherosclerosis thus potentially mitigate both plaque instability fibrosis. Biologic therapies, including monoclonal antibodies that inhibit IL-5, IL-13/IL-4, thymic stromal lymphopoietin, IL-33, IL-17A, show promise exacerbations require close monitoring their immunomodulatory effects. Single-target neutrophil elastase or matrix metalloproteinases limited efficacy aid stabilizing atherosclerotic plaques through promoting vascular smooth muscle cell proliferation. However, tendency degrade extracellular attract immune cells heighten rupture risk, contraindicating use Alpha-1 antitrypsin replacement therapy holds promise, providing protection, especially myocardial injury. Understanding influence these innovative on CVD vital, making it imperative examine molecules at an early stage.
Язык: Английский
Процитировано
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