Fibroblast growth factor 21 alleviates acetaminophen induced acute liver injury by activating Sirt1 mediated autophagy DOI

Guangsen Xu,

Feng Qiu, Wenshu Zhang

et al.

Cellular Signalling, Journal Year: 2024, Volume and Issue: 123, P. 111379 - 111379

Published: Sept. 2, 2024

Language: Английский

Epidermal stem cell derived exosomes-induced dedifferentiation of myofibroblasts inhibits scarring via the miR-203a-3p/PIK3CA axis DOI Creative Commons

Shixin Zhao,

Haoran Kong,

Dahu Qi

et al.

Journal of Nanobiotechnology, Journal Year: 2025, Volume and Issue: 23(1)

Published: Jan. 29, 2025

Hypertrophic scar (HS) is a common fibroproliferative disorders with no fully effective treatments. The conversion of fibroblasts to myofibroblasts known play critical role in HS formation, making it essential identify molecules that promote myofibroblast dedifferentiation and elucidate their underlying mechanisms. In this study, we used comparative transcriptomics single-cell sequencing key pathways mediate fibrosis transdifferentiation. Epidermal stem cell-derived extracellular vesicles (EpiSC-EVs) were isolated via ultracentrifugation filtration, followed by miRNA miRNAs targeting molecules. After vitro vivo treatment EpiSC-EVs, assessed antifibrotic effects through scratch assays, collagen contraction Western blotting, immunofluorescence. Transcriptomic rescue experiments investigate the molecular mechanism which miR-203a-3p EpiSC-EVs induces dedifferentiation. Our results indicate PIK3CA overexpressed tissues positively correlates fibrosis. absorbed scar-derived fibroblasts, promoting from quiescent fibroblasts. Mechanistically, plays an inhibiting expression PI3K/AKT/mTOR pathway hyperactivation, thereby reducing formation. studies confirmed attenuate excessive scarring miR-203a-3p/PIK3CA axis, suggesting as promising therapeutic approach for HS.

Language: Английский

Citations

0

Update of Aging Hallmarks in Idiopathic Pulmonary Fibrosis DOI Creative Commons
Ana Lilia Torres-Machorro,

Ángeles García-Vicente,

Marco Espina-Ordoñez

et al.

Cells, Journal Year: 2025, Volume and Issue: 14(3), P. 222 - 222

Published: Feb. 5, 2025

Idiopathic Pulmonary Fibrosis (IPF) is an epithelial-driven interstitial lung disease of unknown etiology characterized by the excessive proliferation fibroblast populations that synthesize large amounts extracellular matrix. In this devastating disorder, all aging hallmarks appear prematurely or are altered. This review highlights key findings about IPF characteristics recently recognized as aging, including mechanical alterations, inflammaging, dysbiosis, alternative splicing, and disabled macroautophagy. It also revisits classic which encompass stem cell exhaustion, cellular senescence, altered intercellular communication. Enhancing our understanding fundamental processes underlie in may facilitate development innovative experimental strategies to improve therapeutic outcomes.

Language: Английский

Citations

0

Nuciferine Restores Autophagy via the PI3K-AKT-mTOR Pathway to Alleviate Renal Fibrosis in Diabetic Kidney Disease DOI

Tongqing Li,

Huijian Chen,

Yan Guo

et al.

Journal of Agricultural and Food Chemistry, Journal Year: 2025, Volume and Issue: 73(9), P. 5223 - 5235

Published: Feb. 24, 2025

Diabetic kidney disease (DKD) is one of the complications diabetes mellitus, which triggers fibrosis and eventually develops into end-stage renal disease. Nuciferine (NF) most important functional components in lotus leaves (LL), but its role mechanism for treatment DKD are unclear. A high-fat-diet (HFD)-induced model KK-AY mice was established this study. NF significantly improved blood glucose biochemical indices mice. Furthermore, reduced levels mALB, UCRE, Scr, BUN urine. Further, extent lesions study at stage IV according to Mogensen staging method. effective ameliorating injury during period. Concurrently, protein FN, N-cadherin, TGFβ, p-Smad3, p-PI3K, p-AKT, p-mTOR, p62 were decreased. In contrast, level expression Beclin-1 increased. high glucose-exposed HK-2 cell model, p-mTOR all downregulated, autophagy proteins increased after intervention. addition, cells treated with combination Wortmannin 3-MA, respectively. The results demonstrated that inhibited TGFβ p-Smad3 by regulating through PI3K-AKT-mTOR pathway, thereby Therefore, LL can be used as a dietary component prevention patients.

Language: Английский

Citations

0

Particulate matter induces activation of cardiac fibroblasts via HIF1α-mediated autophagy DOI Creative Commons
Zhimin Wang,

Guanghui Hong,

Runting Dou

et al.

Environmental Sciences Europe, Journal Year: 2025, Volume and Issue: 37(1)

Published: March 8, 2025

Language: Английский

Citations

0

Mechanisms and Therapeutic Potential of Myofibroblast Transformation in Pulmonary Fibrosis DOI
Tianming Zhao, Yunchao Su

Deleted Journal, Journal Year: 2025, Volume and Issue: 2(1), P. 10001 - 10001

Published: Jan. 1, 2025

Idiopathic pulmonary fibrosis (IPF) is a progressive, irreversible, and fatal disease with an increasing incidence limited therapeutic options. It characterized by the formation deposition of excess extracellular matrix proteins resulting in gradual replacement normal lung architecture fibrous tissue. The cellular molecular mechanism IPF has not been fully understood. A hallmark fibroblast to myofibroblast transformation (FMT). During excessive repair upon exposure harmful stimuli, fibroblasts transform into myofibroblasts under stimulation cytokines, chemokines, vesicles from various cells. These mediators interact fibroblasts, initiating multiple signaling cascades, such as TGFβ1, MAPK, Wnt/β-catenin, NF-κB, AMPK, endoplasmic reticulum stress, autophagy, contributing FMT. Furthermore, single-cell transcriptomic analysis revealed significant heterogeneity among myofibroblasts, which arise cell types are adapted altered microenvironment during pathological repair. This review provides overview recent research on origins pathways driving their formation, focus interactions between epithelial cells, endothelial macrophages context fibrosis. Based these insights, targeting FMT could offer promising avenues for treatment IPF.

Language: Английский

Citations

0

Idiopathic pulmonary fibrosis microenvironment: Novel mechanisms and research directions DOI Creative Commons
Feng Gao, Lei Pan, Wei Liu

et al.

International Immunopharmacology, Journal Year: 2025, Volume and Issue: 155, P. 114653 - 114653

Published: April 14, 2025

Language: Английский

Citations

0

Integrated bioinformatics analysis screened the key genes and pathways of idiopathic pulmonary fibrosis DOI Creative Commons

Juan Wu,

Yangyang Wei,

Kang Hong

et al.

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

Published: April 25, 2025

Language: Английский

Citations

0

Gluconic acid alleviates hypertrophic scar formation through binding PLOD1, reducing p-AKT signaling and activating autophagy DOI
Jun Li,

Siqi Zeng,

Yue Sun

et al.

Phytomedicine, Journal Year: 2025, Volume and Issue: 143, P. 156825 - 156825

Published: May 1, 2025

Language: Английский

Citations

0

Overexpression of Tgm2 in Chinese Hamster Ovary Cells Enhances Recombinant Monoclonal Antibody Expression and Promotes Cell Proliferation through Reduction of Apoptosis DOI

Huijie Zhang,

Qi Zhao,

Miao Zhang

et al.

ACS Synthetic Biology, Journal Year: 2025, Volume and Issue: unknown

Published: May 6, 2025

Chinese hamster ovary (CHO) cells are the preferred host system for producing protein-based (antibody) therapeutics. However, recombinant CHO undergo substantial apoptosis during prolonged cultivation, impairing cell growth and ultimately compromising product yield quality. Transglutaminase 2 (Tgm2), which mediates post-translational modifications of substrate proteins, regulates critical biological processes including cellular differentiation, apoptosis, cycle progression, extracellular matrix assembly. In this study, we examined effects Tgm2 overexpression knockdown on antibody production. Stable enhanced proliferation while reducing apoptotic rates, resulting in significantly increased adalimumab expression (2.09 ± 0.08-fold) specific productivity (1.88 compared to controls. contrast, promoted induced arrest. Mechanistically, elevated upregulated antiapoptotic genes (Bcl-2, Bcl-xL, Mcl-1) suppressing caspase-3 activity BAX expression. These were associated with PI3K/AKT/mTOR pathway activation. Our findings demonstrate that enhances proliferation, bolsters capacity, improves monoclonal production efficiency cells, establishing it as a viable strategy increasing protein yields.

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