Xinying Jia

Key Laboratory Of Modern Toxicology Of Ministry Of Education
Nanjing, 211166, China

Last Updated: 09/26/2026

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Found 11 publications

FABP5 drives silica-induced myofibroblast senescence and pulmonary fibrosis through a FASN/UCP2 metabolic-mitochondrial axis.

FABP5 drives silica-induced myofibroblast senescence and pulmonary fibrosis through a FASN/UCP2 metabolic-mitochondrial axis.

Journal: Redox biology

Published: June 22, 2026

LEF1 regulated CTHRC1 promotes silica-induced pulmonary fibrosis through CD44-dependent signaling.

LEF1 regulated CTHRC1 promotes silica-induced pulmonary fibrosis through CD44-dependent signaling.

Journal: Toxicology letters

Published: April 23, 2026

Homoharringtonine exerts anti-silicosis potential by inhibiting the CCR1 and PI3K/AKT signaling pathways in lung fibroblasts.

Homoharringtonine exerts anti-silicosis potential by inhibiting the CCR1 and PI3K/AKT signaling pathways in lung fibroblasts.

Journal: Journal of biomedical research

Published: May 21, 2025

NUDT21 regulates lysyl oxidase-like 2(LOXL2) to influence ECM protein cross-linking in silica-induced pulmonary fibrosis.

NUDT21 regulates lysyl oxidase-like 2(LOXL2) to influence ECM protein cross-linking in silica-induced pulmonary fibrosis.

Journal: Ecotoxicology and environmental safety

Published: October 07, 2024

Senescent alveolar type II epithelial cells-secreted GDF15 promotes silicosis progression via interfering intercellular communication.

Senescent alveolar type II epithelial cells-secreted GDF15 promotes silicosis progression via interfering intercellular communication.

Journal: Ecotoxicology and environmental safety

Published: September 18, 2024

Senescent endothelial cell-derived Galectin 3 promotes silicosis through endothelial-fibroblast and endothelial-macrophage crosstalk.

Senescent endothelial cell-derived Galectin 3 promotes silicosis through endothelial-fibroblast and endothelial-macrophage crosstalk.

Journal: Journal of hazardous materials

Published: August 30, 2024

LGALS3 regulates endothelial-to-mesenchymal transition via PI3K/AKT signaling pathway in silica-induced pulmonary fibrosis.

LGALS3 regulates endothelial-to-mesenchymal transition via PI3K/AKT signaling pathway in silica-induced pulmonary fibrosis.

Journal: Toxicology

Published: August 30, 2024

Fatty Acid Oxidation-Glycolysis Metabolic Transition Affects ECM Homeostasis in Silica-Induced Pulmonary Fibrosis.

Fatty Acid Oxidation-Glycolysis Metabolic Transition Affects ECM Homeostasis in Silica-Induced Pulmonary Fibrosis.

Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

Published: June 26, 2024

The interplay of Cxcl10+/Mmp14+ monocytes and Ccl3+ neutrophils proactively mediates silica-induced pulmonary fibrosis.

The interplay of Cxcl10+/Mmp14+ monocytes and Ccl3+ neutrophils proactively mediates silica-induced pulmonary fibrosis.

Journal: Journal of hazardous materials

Published: September 13, 2023

IL33-mediated NPM1 promotes fibroblast-to-myofibroblast transition via ERK/AP-1 signaling in silica-induced pulmonary fibrosis.

IL33-mediated NPM1 promotes fibroblast-to-myofibroblast transition via ERK/AP-1 signaling in silica-induced pulmonary fibrosis.

Journal: Toxicological sciences : an official journal of the Society of Toxicology

Published: July 03, 2023

Associations of combined phenotypic ageing and genetic risk with incidence of chronic respiratory diseases in the UK Biobank: a prospective cohort study.

Associations of combined phenotypic ageing and genetic risk with incidence of chronic respiratory diseases in the UK Biobank: a prospective cohort study.

Journal: The European respiratory journal

Published: February 09, 2023

Showing 1-11 of 11

Last Updated: 09/26/2026