Endothelial Unfolded Protein Response‐Mediated Cytoskeletal Effects DOI
Joy T. Folahan,

Saikat Fakir,

Nektarios Barabutis

et al.

Cell Biochemistry and Function, Journal Year: 2024, Volume and Issue: 42(8)

Published: Oct. 25, 2024

ABSTRACT The endothelial semipermeable monolayers ensure tissue homeostasis, are subjected to a plethora of stimuli, and their function depends on cytoskeletal integrity remodeling. permeability those membranes can fluctuate maintain organ homeostasis. In cases severe injury, inflammation or disease, barrier hyperpermeability cause irreparable damage endothelium‐dependent issues, eventually death. Elucidation the signaling regulating structure promotes development targeted pharmacotherapies towards disorders related impaired endothelium (e.g., acute respiratory distress syndrome, sepsis). Recent reports investigate role unfolded protein response in function. Herein we review components, function; interrelations health disorder. Moreover, emphasize modulators, since they ameliorate illness leak.

Language: Английский

Electrosprayed core–shell microspheres co-deliver fibronectin and resveratrol for combined treatment of acute lung injury DOI
Yifan Huang, Mengsi Zhan, Huxiao Sun

et al.

Journal of Colloid and Interface Science, Journal Year: 2025, Volume and Issue: 686, P. 498 - 508

Published: Jan. 31, 2025

Language: Английский

Citations

2
Neutrophil-derived heparin-binding protein increases endothelial permeability in acute lung injury by promoting TRIM21 and the ubiquitination of P65 DOI Creative Commons
Jian Zhang, Yong Cao,

Wenqi Shu

et al.

Cell Biology and Toxicology, Journal Year: 2025, Volume and Issue: 41(1)

Published: March 5, 2025

Acute lung injury (ALI), which poses a significant public health threat, is commonly caused by sepsis. ALI associated with permeability and glycolysis changes in pulmonary microvascular endothelial cells. Our study demonstrates that heparin-binding protein (HBP), released from neutrophils during sepsis, exacerbates glycolysis, thereby triggering ALI. Through coimmunoprecipitation mass spectrometry, TRIM21 was identified as HBP interaction partner. Notably, enhances the stability of inhibiting K48 ubiquitination. binds to promotes K63-linked ubiquitination P65, facilitating its nuclear translocation. regulates HPMEC manner dependent on P65 stabilizes interactions P65. Rescue experiments conducted vivo vitro demonstrate modulation predominantly mediated through TRIM21-P65 axis. results suggest targeting HBP/TRIM21/P65 axis novel therapeutic strategy ameliorate

Language: Английский

Citations

1
Adaptive bilirubin nanoscavenger alleviates pulmonary oxidative stress and inflammation for acute lung injury therapy DOI Creative Commons
Longfa Kou,

Yitianhe Xu,

Shize Li

et al.

Journal of Advanced Research, Journal Year: 2025, Volume and Issue: unknown

Published: March 1, 2025

Acute lung injury (ALI) is a life-threatening condition characterized by rapidly progressing respiratory distress and hypoxemia. Oxidative stress-induced inflammation in tissue plays crucial role the progression of ALI. Excessive generation reactive oxygen species (ROS) pulmonary microenvironment activates inflammatory signaling pathways, enhancing transcription pro-inflammatory factors ultimately leading to necrosis. Bilirubin (BR), an exceptional endogenous antioxidant, possesses ability counteract elevated levels through direct reactions or inducing antioxidant systems such as Nrf2/HO-1 signaling. However, its limited solubility poses hindrance further applications. Hence, it imperative develop suitable bilirubin-based system for biological utilization. In this study, we developed ROS-sensitive adaptive nanoscavenger (GP@BR) co-assembling bilirubin-conjugated glycol chitosan (GC-BR) polyethylene (PEG-BR), aiming alleviate oxidative stress ALI treatment. The different conjugations endowed bilirubin derivatives with varying sensitivity towards reacting ROS, enabling GP@BR exert antioxidative properties specifically environments on demand. Besides excellent properties, also demonstrated absorb excess cytokines. Moreover, our optimized facilitated transport across mucosal layer epithelial cells. vivo studies confirmed that significantly improved symptoms suppressed fibrosis. This study highlighted potential multiple actions treatment

Language: Английский

Citations

1
Mitophagy and Ferroptosis in Sepsis-Induced ALI/ARDS: Molecular Mechanisms, Interactions and Therapeutic Prospects of Medicinal Plants DOI Creative Commons
Huixin Cheng, Xuehan Wang,

Juyi Yao

et al.

Journal of Inflammation Research, Journal Year: 2024, Volume and Issue: Volume 17, P. 7819 - 7835

Published: Oct. 1, 2024

Sepsis is a common critical illness characterized by high mortality rates and significant disease burden. In the context of sepsis-induced organ dysfunction, lungs are among initial organs affected, which may progress to acute lung injury (ALI) respiratory distress syndrome (ARDS). Recent studies have highlighted crucial roles mitophagy ferroptosis in development progression ALI/ARDS. Identifying key convergence points these processes provide valuable insights for treatment this condition. recent years, certain herbs their bioactive compounds demonstrated unique benefits managing ALI/ARDS modulating or ferroptosis. This review summary mechanisms ferroptosis, explores interactions, emphasizes regulatory Additionally, it offers novel perspective on strategies summarizing various relevant

Language: Английский

Citations

4
Macrophages in sepsis-induced acute lung injury: exosomal modulation and therapeutic potential DOI Creative Commons

Kangzheng Lv,

Qun Liang

Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 15

Published: Jan. 7, 2025

Sepsis-induced acute lung injury (ALI) remains a leading cause of mortality in critically ill patients. Macrophages, key modulators immune responses, play dual role both promoting and resolving inflammation. Exosomes, small extracellular vesicles released by various cells, carry bioactive molecules that influence macrophage polarization responses. Emerging researchers have identified exosomes as crucial mediators modulate activity during sepsis-induced ALI. This review explores the modulating functions, focusing on cellular interactions within microenvironment their potential therapeutic targets. It highlights regulation macrophages derived from pathogenic germs, neutrophils, alveolar epithelial mesenchymal stromal cells. By understanding these mechanisms, it aims to uncover innovative strategies for

Language: Английский

Citations

0
Cell-cell crosstalk in the pathogenesis of acute lung injury and acute respiratory distress syndrome DOI

Zhenzhen Zhu,

Ying Zhang, Huan Chen

et al.

Tissue Barriers, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 11, 2025

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are the result of an exaggerated inflammatory response triggered by a variety pulmonary systemic insults. The tissues comprised cell types, including alveolar epithelial cells, vascular endothelial macrophages, neutrophils, others. There is mounting evidence that these diverse populations within interact to regulate inflammation in both direct indirect stimuli. aim this review provide summary discussion recent advances understanding importance cell-cell crosstalk pathogenesis ALI/ARDS, with specific focus on interactions may offer prospective therapeutic avenues for ALI/ARDS.

Language: Английский

Citations

0
TREM2 alleviates sepsis-induced acute lung injury by attenuating ferroptosis via the SHP1/STAT3 pathway DOI
Siyi Wu,

Yuanjie He,

Jiemei Li

et al.

Free Radical Biology and Medicine, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 1, 2025

Language: Английский

Citations

0
E3 ubiquitin ligase TRIM7 alleviates LPS-induced acute lung injury via inhibiting NLRP3 inflammasome activation DOI

Youna Wang,

Xiaohong Xu, Peng Zhang

et al.

American Journal Of Pathology, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 1, 2025

Language: Английский

Citations

0
Sepsis subphenotypes: bridging the gaps in sepsis treatment strategies DOI Creative Commons
Xue Zhang, Wei Zhang, Huan Zhang

et al.

Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16

Published: Feb. 6, 2025

Sepsis, a heterogeneous illness produced by dysregulated host response to infection, remains severe mortality risk. Recent discoveries in sepsis research have stressed phenotyping as feasible strategy for tackling heterogeneity and enhancing therapy precision. Sepsis has moved from traditional stratifications based on severity prognosis dynamic, phenotype-driven therapeutic options. This review covers recent progress connecting subgroups personalized treatments, with focus phenotype-based predictions decision-support systems. Despite ongoing challenges, such standardizing frameworks incorporating findings into clinical practice, this topic enormous promise. By investigating phenotypic variation responses, we hope uncover new biomarkers solutions, laying the groundwork more effective therapies and, ultimately improving patient outcomes.

Language: Английский

Citations

0
Reprogramming Lung Redox Homeostasis by NIR Driven Ultra‐Small Pd Loaded Covalent Organic Framework Inhibits NF‐κB Pathway for Acute Lung Injury Immunotherapy DOI Creative Commons

Doudou Lei,

Lin Liao, Tao Qin

et al.

Advanced Science, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 18, 2025

Abstract Acute lung injury (ALI) refers to damage related cells, typically caused by an uncontrollable inflammatory response, and over‐generated reactive oxygen species (ROS). Increasing evidence suggests that reprogramming redox homeostasis holds significant potentials for the clinical treatment of ALI. Herein, simple synthesis ultra‐small Pd loaded covalent organic framework (COF) (TP@Pd) is reported, which, when combined with near infrared (NIR) irradiation, exhibits nanozyme functionalities, including multiple enzyme mimicking activities broad spectrum ROS scavenging, thereby promoting tissue repair ALI immunotherapy. Mechanistically, through therapeutic strategy TP@Pd+NIR, damaged cells tissues are ameliorated decreasing intracellular levels (total ROS, ·OH ·O 2 − ), downregulating cytokines (IL‐6, TNF‐α IL‐1β), upregulating antioxidant factor level (SOD2), inducing macrophage M2 directional polarization (downregulation iNOS CD86, upregulation IL‐10 CD206), activating immunoregulation (CD4 + /CD8 ratio increase), (upregulation HSP70 CD31), suppressing NF‐κB signaling pathway phosphorylated p65 IκBα). Furthermore, following intravenous (IV) injection in rats, TP@Pd accumulated 6 h, indicating promising efficacy via this administration route. Notably, TP@Pd+NIR demonstrated excellent synergistic effects alleviating inflammation storms, reducing diffuse alveolar damage, accelerating repair. Summarily, work has designed a novel enhancement amelioration, which may serve as approach other diseases.

Language: Английский

Citations

0