The impact of glucose metabolism on inflammatory processes in sepsis-induced acute lung injury DOI Creative Commons

Shilei Cheng,

Yufei Li, Xiaoliang Sun

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Dec. 6, 2024

Acute lung injury (ALI) is a prevalent and critical complication of sepsis, marked by high incidence mortality rates, with its pathogenesis still not being fully elucidated. Recent research has revealed significant correlation between the metabolic reprogramming glucose sepsis-associated ALI (S-ALI). Throughout course S-ALI, immune cells, including macrophages dendritic undergo shifts to accommodate intricate demands function that emerge as sepsis advances. Indeed, in S-ALI serves double-edged sword, fueling inflammatory responses initial stages subsequently initiating anti-inflammatory disease evolves. In this review, we delineate current progress concerning pathogenic mechanisms linked focus on pertinent cells implicated. We encapsulate impact onset, progression, prognosis S-ALI. Ultimately, examining key regulatory factors within intermediates enzymes, have identified potential therapeutic targets reprogramming, striving tackle inherent challenges diagnosing treating Severe Lung Injury (S-ALI) greater efficacy.

Language: Английский

Identification of shared important genes associated with ferroptosis across different etiologies of acute lung injury DOI Creative Commons
Jing Li, Yuan‐Han Yang,

Zhengjun Cui

et al.

Scientific Reports, Journal Year: 2025, Volume and Issue: 15(1)

Published: April 19, 2025

Acute lung injury (ALI) of different etiologies has shared pathophysiologic process, from which we speculated that ALI may share common molecular features. While the genetic characteristics remain unclear. In this paper, aimed to identify ferroptosis-associated and bottleneck genes acute etiologies. Firstly, extracted five groups gene sets related three distinct models Gene Expression Omnibus (GEO) database. Then, through utilization weighted co-expression network analysis (WGCNA), identified 3 significant modules ascertained 7 co-expressed affected by these models. Subsequently, differential expression protein-protein interaction for modules, Slc7a11 was identified. Moreover, subjected were used via FerrDb Finally, key confirmed validated. addition, observed is both a driver suppressor in Interestingly, found level significantly upregulated Experimentally, rat tissues using immunofluorescence staining real-time polymerase chain reaction (qRT-PCR) assays. Collectively, our findings complement exploration pathogenesis ALI. There are features etiology increased ALI, can improve understanding mechanisms underlying

Language: Английский

Citations

0
Ferroptosis targeting offers a Therapeutic Target for Septic cardiomyopathy DOI
Ping Zhou, Mengxue Liu, Tao Lv

et al.

Tissue and Cell, Journal Year: 2025, Volume and Issue: 95, P. 102930 - 102930

Published: April 25, 2025

Language: Английский

Citations

0
Systematic analysis of molecules regulating nitric oxide (NO) metabolism and vascular endothelium condition DOI Creative Commons
I. Yu. Torshin, А. Г. Чучалин, О. А. Громова

et al.

FARMAKOEKONOMIKA Modern Pharmacoeconomics and Pharmacoepidemiology, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 25, 2025

Background. Nitric monooxide (NO) is a signaling molecule that plays an important role in many physiological processes, including the regulation of vascular tone, neurotransmission, immunity, mitochondrial respiration, and skeletal muscle contractility. Certain molecules, which are micronutrients or active ingredients number drugs, improve biosynthesis secretion NO. Objective: systematization information on impact various molecules modulation NO levels normal pathological conditions. Material methods. An array all currently available publications fundamental clinical studies effects was studied. By query “nitric oxide” PubMed/MEDLINE database biomedical 198,480 articles were detected, by oxide AND endothelium” 27,869 found (with peak 2005). After loading this sample, systematic analysis these performed using topological metric approaches. Results. This paper presents results issue, allowed us to identify at least 123 that, one way another, modulate body. Molecules metabolism can be conditionally divided into four groups: (1) macro- micronutrients; (2) components natural extracts; (3) medicines; (4) affect nitric through reparation glycocalyx damage. Of above variety endothelium biosynthesis, sulodexide stands out (by its effect glycocalyx). Conclusion. The use (a mixture glycosaminoglycans with high degree pharmaceutical standardization) promising areas therapy for endothelial dysfunction restoration glycocalyx, accompanied biosynthesis.

Language: Английский

Citations

0
Modulating the NLRP3 Inflammasome: Acitretin as a potential treatment for Sepsis-induced acute lung injury DOI Creative Commons

Huikang Xu,

Haowen Xu,

Weifeng Li

et al.

International Immunopharmacology, Journal Year: 2025, Volume and Issue: 153, P. 114504 - 114504

Published: April 1, 2025

Acitretin, a well-established dermatological drug primarily used for psoriasis treatment, has been clinically several decades. However, its potential role in modulating inflammation sepsis remains unexplored. This study seeks to explore the impact of acitretin on sepsis-induced acute lung injury (ALI) and elucidate underlying mechanisms involved. In mouse model induced by lipopolysaccharide (LPS), we assessed effects ALI. Transcriptome sequencing tissue was performed identify relevant signaling pathways. vitro, bone marrow-derived macrophages (BMDMs) were treated with (1 μM, 5 μM 10 μM) evaluate NOD-, LRR- pyrin domain-containing protein 3(NLRP3) inflammasome activation pyroptosis. vivo, wild-type, Nlrp3 knockout, Gsdmd knockout mice confirm NLRP3 mediating acitretin's effects. Acitretin significantly mitigated ALI, reducing mortality LPS-challenged mice. analysis revealed that suppressed pathway tissue. dose-dependently inhibited interleukin (IL)-1β release, caspase-1 p20 production, GSDMD cleavage BMDMs. Furthermore, preventing ASC oligomerization interaction NLRP3. reduced inflammation, IL-1β levels bronchoalveolar lavage fluid, ratio wet dry wide-type mice, but these abolished demonstrated significant anti-inflammatory properties through suppression inflammasome, suggesting as therapeutic strategy related complications.

Language: Английский

Citations

0
On the influence of glycocalyx on NO biosynthesis: The role of sulodexide DOI Creative Commons
О. А. Громова, I. Yu. Torshin, А. Г. Чучалин

et al.

Meditsinskiy sovet = Medical Council, Journal Year: 2025, Volume and Issue: 5, P. 196 - 205

Published: May 4, 2025

The glycocalyx is a special ultra-fine structure of glycosaminoand proteoglycans, 0.2–5 μm thick, covering the endothelium. Maintenance mechanisms synthesis and secretion signaling molecule NO, this regulator vascular tone, mitochondrial respiration, neurotransmission immunity, occurs through reconstruction glycocalyx. Sulodexide combination natural glycosaminoglycans – heparan sulfate dermatan sulfate, which are part antithrombotic effect sulodexide, realized suppression platelet adhesion aggregation, mild anticoagulant profibrinolytic effects, well known. In addition to prevention thrombus formation, use sulodexide one important areas endothelial dysfunction therapy restoration NO biosynthesis. Evidence shows that promising for treatment both arterial venous thrombotic disorders in patients with type 2 diabetes mellitus (T2DM), hypertension (AH), coronavirus infection COVID-19, after surgery, thrombophilia, etc. A meta-analysis study data demonstrates reduced risk death from cardiovascular causes sulodexide. As personalized prescription results diagnostics should be taken into account. If patient has events, anticoagulants antiplatelet agents used accordance clinical guidelines. properties characterized by low level bleeding; it when impossible high bleeding, as if hypertension, diabetes, chronic diseases, diseases arteries lower extremities.

Language: Английский

Citations

0
Focus on the role of calcium signaling in ferroptosis: a potential therapeutic strategy for sepsis-induced acute lung injury DOI Creative Commons
Yifei Xu,

Xintian Qu,

Minghao Liang

et al.

Frontiers in Medicine, Journal Year: 2024, Volume and Issue: 11

Published: Sept. 17, 2024

By engaging in redox processes, ferroptosis plays a crucial role sepsis-induced acute lung injury (ALI). Although iron stimulates calcium signaling through the stimulation of redox-sensitive pathways, function signals physiological process septic ALI remains unidentified. Iron homeostasis disequilibrium is frequently accompanied by aberrant signaling. Intracellular overflow can be symptom dysregulation cellular state, which characterized overload during early phase ferroptosis. This lead to disruptions and The mechanisms controlling are reviewed here, along with their significance injury, potential these processes clarified. We propose that development combined involving bidirectional interaction between Our goal raise awareness about pathophysiology investigate relationship also aimed develop calcium-antagonistic therapies target improve quality survival for patients suffering from injury.

Language: Английский

Citations

1
The impact of glucose metabolism on inflammatory processes in sepsis-induced acute lung injury DOI Creative Commons

Shilei Cheng,

Yufei Li, Xiaoliang Sun

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Dec. 6, 2024

Acute lung injury (ALI) is a prevalent and critical complication of sepsis, marked by high incidence mortality rates, with its pathogenesis still not being fully elucidated. Recent research has revealed significant correlation between the metabolic reprogramming glucose sepsis-associated ALI (S-ALI). Throughout course S-ALI, immune cells, including macrophages dendritic undergo shifts to accommodate intricate demands function that emerge as sepsis advances. Indeed, in S-ALI serves double-edged sword, fueling inflammatory responses initial stages subsequently initiating anti-inflammatory disease evolves. In this review, we delineate current progress concerning pathogenic mechanisms linked focus on pertinent cells implicated. We encapsulate impact onset, progression, prognosis S-ALI. Ultimately, examining key regulatory factors within intermediates enzymes, have identified potential therapeutic targets reprogramming, striving tackle inherent challenges diagnosing treating Severe Lung Injury (S-ALI) greater efficacy.

Language: Английский

Citations

1