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

Network Pharmacology-driven therapeutic interventions for Interstitial Lung Diseases using Traditional medicines: A Narrative Review DOI Creative Commons
Megh Pravin Vithalkar, K. Sandra,

Bharath Harohalli Byregowda

et al.

International Immunopharmacology, Journal Year: 2025, Volume and Issue: 147, P. 113979 - 113979

Published: Jan. 1, 2025

This review explores the progressive domain of network pharmacology and its potential to revolutionize therapeutic approaches for Interstitial Lung Diseases (ILDs), a collective term encompassing Pneumonia, Pneumoconiosis, Connective Tissue Disease-related ILDs, Sarcoidosis. The exploration focuses on profound legacy traditional medicines, particularly Ayurveda Traditional Chinese Medicines (TCM), their largely unexplored capacity in ILD treatment. These ancient healing systems, characterized by holistic methodologies multifaceted treatment modalities, offer promising foundation discovering innovative strategies. Moreover, underscores amalgamation artificial intelligence (AI) machine learning (ML) with bioinformatics, creating computational synergy capable deciphering intricate biological networks associated ILDs. Network has tailored hypothesis from conventional "one target, one drug" towards "network multi-component therapeutics" approach. fusion literature technology can unveil novel drugs, targets, pathways, augmenting effective therapies diminishing adverse effects related current medications. In conclusion, this provides comprehensive exposition how Pharmacology tools leverage insights TCM craft efficacious solutions It sets stage future investigations captivating interdisciplinary domain, validating use medicines worldwide.

Language: Английский

Citations

1

Astragaloside IV promotes neuronal axon regeneration by inhibiting the PTEN/AKT pathway DOI
Luning Lin, Chenyang Zhao, Huijuan Lv

et al.

Brain Research, Journal Year: 2025, Volume and Issue: 1850, P. 149451 - 149451

Published: Jan. 8, 2025

Language: Английский

Citations

1

Revisiting the role of MicroRNAs in the pathogenesis of idiopathic pulmonary fibrosis DOI Creative Commons
Zhimin Zhou,

Yuhong Xie,

Qianru Wei

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2024, Volume and Issue: 12

Published: Oct. 16, 2024

Idiopathic pulmonary fibrosis (IPF) is a prevalent chronic disease characterized by alveolar epithelial cell damage, fibroblast proliferation and activation, excessive extracellular matrix deposition, abnormal epithelial-mesenchymal transition (EMT), resulting in tissue remodeling irreversible structural distortion. The mortality rate of IPF very high, with median survival time 2–3 years after diagnosis. exact cause remains unknown, but increasing evidence supports the central role epigenetic changes, particularly microRNA (miRNA), IPF. Approximately 10% miRNAs lung exhibit differential expression compared to normal tissue. Diverse miRNA phenotypes exert either pro-fibrotic or anti-fibrotic influence on progression In context IPF, factors such as DNA methylation long non-coding RNAs (lncRNAs) regulate differentially expressed miRNAs, which turn modulate various signaling pathways implicated this process, including transforming growth factor-β1 (TGF-β1)/Smad, mitogen-activated protein kinase (MAPK), phosphatidylinositol-3-kinase/protein B (PI3K/AKT) pathways. Therefore, review presents epidemiology discusses multifaceted regulatory roles explores impact through pathways, TGF-β1/Smad pathway its constituent structures. Consequently, we investigate potential for targeting treatment thereby contributing advancements research.

Language: Английский

Citations

5

Cis-3-hexenal modulates 3-hydroxy-3-methylglutaryl-CoA reductase at multiple levels to enhance triterpenoid production in the root cultures of Astragalus mongholicus Bunge DOI Creative Commons
Haifeng Sun, Zhi Gao,

J Zhang

et al.

Industrial Crops and Products, Journal Year: 2025, Volume and Issue: 230, P. 121066 - 121066

Published: April 30, 2025

Language: Английский

Citations

0

Understanding the molecular regulatory mechanisms of autophagy in lung disease pathogenesis DOI Creative Commons
Lin Lin,

Yumeng Lin,

Zhongyu Han

et al.

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

Published: Oct. 31, 2024

Lung disease development involves multiple cellular processes, including inflammation, cell death, and proliferation. Research increasingly indicates that autophagy its regulatory proteins can influence programmed proliferation, innate immune responses. Autophagy plays a vital role in the maintenance of homeostasis adaptation eukaryotic cells to stress by enabling chelation, transport, degradation subcellular components, organelles. This process is essential for sustaining balance ensuring health mitochondrial population. Recent studies have begun explore connection between different lung diseases. article reviews latest findings on molecular mechanisms diseases, with an emphasis potential targeted therapies autophagy.

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