Blockade of TREM-1 alleviates alveolar epithelial cell senescence through Nrf2-mediated antioxidant pathways in pulmonary fibrosis DOI Creative Commons
Jian‐Bing Xiong, Chen‐Yu Zhang, Ling Jin

et al.

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 27, 2024

Abstract Our previous study showed that blocking triggering receptors expressed on myeloid cell-1 (TREM-1) attenuate bleomycin (BLM)-induced pulmonary fibrosis (PF) in mice. However, its underlying mechanism remains unclear. Here, we found blockade of TREM-1 during the fibrotic phase attenuated BLM-induced PF mice, with less expression senescence-relative protein, including p16, p21, p53, and γ-H2AX lung tissue. Moreover, stage restored anti-oxidant levels by increasing percentage Nrf2- HO-1-positive cells Notably, was highly SFTPC-positive alveolar epithelial (AECs) In vitro, activated Nrf2 signaling, thereby decreasing intracellular ROS diminishing senescence AECs. Furthermore, inhibition Nrf2/HO-1 partially counteracted anti-senescence effect BLM treated-AECs. In conclusion, our findings elucidate new insights into molecular mechanisms associated AEC pathogenesis PF.

Language: Английский

Prognostic Function and Immunologic Landscape of a Predictive Model Based on Five Senescence-Related Genes in IPF Bronchoalveolar Lavage Fluid DOI Creative Commons
Cheng Zhong, Yuqiong Lei, Jingyuan Zhang

et al.

Biomedicines, Journal Year: 2024, Volume and Issue: 12(6), P. 1246 - 1246

Published: June 3, 2024

Background: Idiopathic pulmonary fibrosis (IPF) is a type of interstitial lung disease characterized by unknown causes and poor prognosis. Recent research indicates that age-related mechanisms, such as cellular senescence, may play role in the development this condition. However, relationship between senescence clinical outcomes IPF remains uncertain. Methods: Data from GSE70867 database were meticulously analyzed study. The employed differential expression analysis, well univariate multivariate Cox regression to pinpoint senescence-related genes (SRGs) linked prognosis construct prognostic risk model. model’s relevance its connection potential biological processes systematically assessed training testing datasets. Additionally, location prognosis-related SRGs was identified through immunohistochemical staining, correlation immune cell infiltration deduced using GSE28221 dataset. Result: model constructed based on five (cellular communication network factor 1, CYR61, stratifin, SFN, megakaryocyte-associated tyrosine kinase, MATK, C-X-C motif chemokine ligand CXCL1, LIM domain, actin binding LIMA1). Both Kaplan-Meier (KM) curves (p = 0.005) time-dependent receiver operating characteristic (ROC) analysis affirmed predictive accuracy datasets, with respective areas under ROC curve at 1-, 2-, 3-years being 0.721, 0.802, 0.739. Furthermore, qRT-RCR staining verify samples controls. Moreover, patients high-risk group contained higher levels neutrophils, eosinophils, M1 macrophages BALF, which appeared be independent indicators patients. Conclusion: Our reveals effectiveness 5 BALF for stratification prediction patients, providing new insights into progression.

Language: Английский

Citations

0
Carvacrol protects rats against bleomycin-induced lung oxidative stress, inflammation, and fibrosis DOI
Marzieh Pashmforosh, Hossein Rajabi Vardanjani, Layasadat Khorsandi

et al.

Naunyn-Schmiedeberg s Archives of Pharmacology, Journal Year: 2024, Volume and Issue: 397(12), P. 10075 - 10089

Published: July 8, 2024

Language: Английский

Citations

0
Genetically engineered biomimetic ATP-responsive nanozyme for the treatment of cardiac fibrosis DOI
Xueli Zhao,

Yuze Qin,

Bowen Li

et al.

Published: Oct. 30, 2024

Abstract Background Cardiac fibrosis plays a critical role in the progression of various forms heart disease, significantly increasing risk sudden cardiac death. However, there are presently no therapeutic strategies available to prevent onset fibrosis. Methods and Results Here, biomimetic ATP-responsive nanozymes based on genetically engineered cell membranes adapted specifically recognize activated fibroblasts (CFs) for treatment By fusing anti FAP-Car membrane zeolitic imidazole frameworks-90 (zif-90) cores loaded with antioxidant CeO2 siCTGF, these nanoparticles, called FM@zif-90/Ce/siR NPs, demonstrated effectively reduce accumulation myofibroblasts formation fibrotic tissue, while restoring function. Conclusions These findings demonstrate that combination siCTGF has beneficial curative effect fibrosis, significant translational potential.

Language: Английский

Citations

0
Extracellular Vesicles in Idiopathic Pulmonary Fibrosis: Pathogenesis, Biomarkers and Innovative Therapeutic Strategies DOI Creative Commons
Yanbin Yang, Mengen Lv, Qingsong Xu

et al.

International Journal of Nanomedicine, Journal Year: 2024, Volume and Issue: Volume 19, P. 12593 - 12614

Published: Nov. 1, 2024

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and irreversible interstitial lung disease caused by aberrant deposition of extracellular matrix in the lungs with significant morbidity mortality. The therapeutic choices for IPF remain limited. Extracellular vesicles (EVs), as messengers intercellular communication, are cell-secreted lipid bilayer nanoscale particles found body fluids, regulate epithelial phenotype profibrotic signaling pathways transporting bioactive cargo to recipients pathogenesis IPF. Furthermore, an increasing number studies suggests that EVs derived from stem cells can be employed cell-free approach IPF, given their intrinsic tissue-homing capabilities regeneration characteristics. This review highlights new sights potential diagnostic prognostic biomarkers, prospects novel drug delivery systems next-generation therapeutics against Notably, bringing engineering strategies holds great promise enhancing effect anti-pulmonary promoting clinical transformation.

Language: Английский

Citations

0
Blockade of TREM-1 alleviates alveolar epithelial cell senescence through Nrf2-mediated antioxidant pathways in pulmonary fibrosis DOI Creative Commons
Jian‐Bing Xiong, Chen‐Yu Zhang, Ling Jin

et al.

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 27, 2024

Abstract Our previous study showed that blocking triggering receptors expressed on myeloid cell-1 (TREM-1) attenuate bleomycin (BLM)-induced pulmonary fibrosis (PF) in mice. However, its underlying mechanism remains unclear. Here, we found blockade of TREM-1 during the fibrotic phase attenuated BLM-induced PF mice, with less expression senescence-relative protein, including p16, p21, p53, and γ-H2AX lung tissue. Moreover, stage restored anti-oxidant levels by increasing percentage Nrf2- HO-1-positive cells Notably, was highly SFTPC-positive alveolar epithelial (AECs) In vitro, activated Nrf2 signaling, thereby decreasing intracellular ROS diminishing senescence AECs. Furthermore, inhibition Nrf2/HO-1 partially counteracted anti-senescence effect BLM treated-AECs. In conclusion, our findings elucidate new insights into molecular mechanisms associated AEC pathogenesis PF.

Language: Английский

Citations

0