Non-Structural Protein V of Canine Distemper Virus Induces Autophagy via PI3K/AKT/mTOR Pathway to Facilitate Viral Replication DOI Open Access
Xin Tian, Rui Zhang,

Shuang Yi

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 26(1), P. 84 - 84

Published: Dec. 25, 2024

Canine distemper (CD) is a highly infectious disease of dogs which caused by canine virus (CDV). Previous studies have demonstrated that CDV infection can induce autophagy in cells. However, the mechanism underlying CDV-induced remains not fully understood. The non-structural protein V plays vital role viral replication and pathogenicity host. In this study, we investigated relationship between CDV-V induction further explored its impact on behind this. Our results showed induced via inhibiting phosphorylation PI3K, AKT, mTOR to promote replication. activation or inhibition PI3K resulted enhancing reducing replication, respectively. Further revealed interacted with cellular autophagy. present study PI3K/AKT signaling pathway enhance improve understanding molecular offer new perspectives for development effective treatment prevention strategies.

Language: Английский

Role and mechanisms of autophagy, ferroptosis, and pyroptosis in sepsis-induced acute lung injury DOI Creative Commons

Yao Shen,

Yingying He, Ying Pan

et al.

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

Published: Aug. 5, 2024

Sepsis-induced acute lung injury (ALI) is a major cause of death among patients with sepsis in intensive care units. By analyzing model sepsis-induced ALI using lipopolysaccharide (LPS) and cecal ligation puncture (CLP), treatment methods strategies to protect against were discussed, which could provide an experimental basis for the clinical ALI. Recent studies have found that imbalance autophagy, ferroptosis, pyroptosis key mechanism triggers ALI, regulating these mechanisms can improve injuries caused by LPS or CLP. This article summarized reviewed regulatory networks their important roles process LPS/CLP-induced sepsis, discusses possible targeted drugs above effects, describes dilemma prospects, provides new perspectives future

Language: Английский

Citations

8
From immune dysregulation to organ dysfunction: understanding the enigma of Sepsis DOI Creative Commons
Zhi Liu, Ting Yuan, Miao Li

et al.

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

Published: Aug. 26, 2024

Sepsis is a syndrome precipitated by immune dysregulation in response to infection, and represents pivotal factor global mortality attributed diseases. The recent consensus delineates sepsis as perilous state of organ dysfunction arising from the host’s maladaptive reaction infection. It masks complexity breadth mechanisms involved sepsis, which characterized simultaneous hyperinflammation immunosuppression. highly correlated with response, mainly mediated various cells their interactions. This can lead plethora complications, encompassing systemic inflammatory metabolic disturbances, infectious shock, MODS, DIC. Furthermore, more research studies have been conducted on past few years. pathological characteristics improved or treated targeting signaling pathways like NF-B, JAK–STAT, PI3K-Akt, p38-MAPK. Combined drug therapy better than single for sepsis. article will review latest progress pathogenesis treatment

Language: Английский

Citations

8
3-methyladenine ameliorates acute lung injury by inhibiting oxidative damage and apoptosis DOI Creative Commons

Xiong Lei,

Xiling Liu, Jia Yu

et al.

Heliyon, Journal Year: 2024, Volume and Issue: 10(13), P. e33996 - e33996

Published: July 1, 2024

Acute lung injury (ALI) is a condition characterized by inflammation and oxidative damage. 3-methyladenine (3-MA) has great potential for regulating apoptosis, but its regulatory role in ALI unknown.

Language: Английский

Citations

3
Ginsenoside Rb1 targets to HO-1 to improve sepsis by inhibiting ferroptosis DOI
Shasha He, Haoran Ye, Qian Wang

et al.

Free Radical Biology and Medicine, Journal Year: 2024, Volume and Issue: 226, P. 13 - 28

Published: Nov. 6, 2024

Language: Английский

Citations

3
Alleviation of LPS-induced sepsis lung injury by propolis-based nanocomposites through the TLR4/NFKB and P2X7/AKT pathways DOI
Hilal Üstündağ, Adem Kara, Necip Gökhan Taş

et al.

Toxicon, Journal Year: 2025, Volume and Issue: unknown, P. 108330 - 108330

Published: March 1, 2025

Language: Английский

Citations

0
Advances in sepsis research: Insights into signaling pathways, organ failure, and emerging intervention strategies DOI Creative Commons
Yehua Li, Siying Ren,

Shenao Zhou

et al.

Experimental and Molecular Pathology, Journal Year: 2025, Volume and Issue: 142, P. 104963 - 104963

Published: March 27, 2025

Language: Английский

Citations

0
PICK1 overexpression ameliorates endotoxin-induced acute lung injury by regulating mitochondrial quality control via maintaining Nrf-2 stabilization through activating the PI3K/Akt/GSK-3β pathway and disrupting the E3 ubiquitin ligase adapter β-TrCP DOI

Meizi Qian,

Yurun Zhu,

Wen-Lang Lin

et al.

International Immunopharmacology, Journal Year: 2025, Volume and Issue: 156, P. 114685 - 114685

Published: April 25, 2025

Language: Английский

Citations

0
Control of inflammatory lung injury and repair by metabolic signaling in endothelial cells DOI

S. E. Gould,

Aretha Herron,

Jonathan Davis

et al.

Current Opinion in Hematology, Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 18, 2024

Purpose of review Sepsis-induced inflammatory lung injury includes acute (ALI) and respiratory distress syndrome (ARDS). There are currently no effective treatments for ALI/ARDS, but clinical outcomes could be improved by inhibiting and/or promoting post-sepsis vascular repair. In this review, we describe studies endothelial cell metabolic pathways in sepsis-induced ALI/ARDS repair identify areas research that deserve attention future studies. We also interventions aim to inhibit promote repair, including those target metabolites, signaling pathways, metabolism. Recent findings Endothelial cells integral both the phases ALI/ARDS. During phase survival decreases, cell-to-endothelial (EC-EC) junctions weakened. after injury, proliferation EC-EC junction reannealing occur. These crucial aspects is, viability, growth, integrity, controlled a myriad metabolites cells. Summary Metabolic represent novel class putative targets prevention treatment injury. Therapies being explored as potential

Language: Английский

Citations

1
LL37-mtDNA regulates viability, apoptosis, inflammation, and autophagy in lipopolysaccharide-treated RLE-6TN cells by targeting Hsp90aa1 DOI Creative Commons

Yunlong Zuo,

Run Dang,

Hongyan Peng

et al.

Open Life Sciences, Journal Year: 2024, Volume and Issue: 19(1)

Published: Jan. 1, 2024

Sepsis-induced acute lung injury is associated with epithelial cell injury. This study analyzed the role of antimicrobial peptide LL37 mitochondrial DNA (LL37-mtDNA) and its potential mechanism action in lipopolysaccharide (LPS)-treated rat type II alveolar cells (RLE-6TN cells). RLE-6TN were treated LPS alone or LL37-mtDNA, followed by transcriptome sequencing. Differentially expressed pivotal genes screened using bioinformatics tools. The effects LL37-mtDNA on viability, inflammation, apoptosis, reactive oxygen species (ROS) production, autophagy-related hallmark expression evaluated LPS-treated cells. Additionally, Hsp90aa1 silencing following treatment investigated vitro. further suppressed augmented promoted release inflammatory cytokines, increased ROS elevated LC3B Using sequencing bioinformatics, ten candidate identified, which three core verified to be upregulated + group. downregulation attenuated possibly acted as a crucial target counteract autophagy activation

Language: Английский

Citations

0
Dihydropashanone Isolated from Lindera erythrocarpa, a Potential Natural Product for the Treatment of Neurodegenerative Diseases DOI Open Access
Zhiming Liu,

Chi–Su Yoon,

Hwan Lee

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(5), P. 2545 - 2545

Published: Feb. 22, 2024

Lindera erythrocarpa, a flowering plant native to eastern Asia, has been reported have neuroprotective activity. However, reports on the specific bioactive compounds in L. erythrocarpa are finite. The aim of this study was investigate anti-neuroinflammatory and effects isolated from erythrocarpa. Dihydropashanone, compound extract, found protected mouse hippocampus HT22 cells glutamate-induced cell death. antioxidant anti-inflammatory properties dihydropashanone microglial BV2 were explored study. results reveal that inhibits lipopolysaccharide-induced inflammatory response suppresses activation nuclear factor (NF)-κB cells. In addition, reduced buildup reactive oxygen species induced E2-related 2 (Nrf2)/heme oxygenase (HO)-1 signaling pathway Our suggest reduces neuroinflammation by decreasing NF-κB microglia protects neurons oxidative stress via Nrf2/HO-1 pathway. Thus, our data offers broad range applications treatment neurodegenerative illnesses.

Language: Английский

Citations

0