ArticleInternational journal of environmental research and public health2022
Inhibition of HIF-1α Attenuates Silica-Induced Pulmonary Fibrosis.
Article in International journal of environmental research and public health, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- Attenuating amiodarone-induced lung toxicity by the vitamin D receptor activator paricalcitol in rats: targeting TLR4/NF-κB/HIF-1α and TGF-β/Smad signaling pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Yizong Tongluo formula attenuates idiopathic pulmonary fibrosis and inflammatory injury by inhibiting HIF-1α/LSH/SCD1-mediated ferroptosis.Frontiers in immunology · 2026Article
- 4EBP1 phosphorylation mediates TGF-β1-induced hepatic fibrosis and upregulates HIF-1α expression.iScience · 2025Article
- HIF-1α-mediated inhibition of the sFlt-1/sENG/TNF-α pathway promotes angiogenesis to ameliorate pre-eclampsia.Journal of molecular histology · 2025Article
- Article
- Developments in the study of the role of lactate metabolism in the genesis and progression of thyroid cancer.Frontiers in cell and developmental biology · 2025Review
- Hydrogen sulfide alleviates high-salt-stimulated myocardial fibrosis through inhibiting hypoxia-inducible factor-1α.Frontiers in pharmacology · 2025Article
- Exposure of Primary Human Skin Fibroblasts to Carbon Dioxide-Containing Solution Significantly Reduces TGF-β-Induced Myofibroblast Differentiation In Vitro.International journal of molecular sciences · 2024Article
- The role of Sirtuin 1 in regulation of fibrotic genes expression in pre-adipocytes.Journal of diabetes and metabolic disorders · 2024Article
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13 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundExcessive accumulation of extracellular matrix is a key feature of pulmonary fibrosis (PF), and myofibroblasts are the main producers of extracellular matrix. Fibroblasts are the major source of myofibroblasts, but the mechanisms of transdifferentiation are unclear.
methodsIn vitro, transforming growth factor-β1 was used to induce NIH-3T3 cell transdifferentiation. DMOG was used to increase hypoxia-inducible factor-1α subunit (HIF-1α) expression. KC7F2 and siRNA decreased HIF-1α expression. In vivo, silica particles were used to induce PF in C57BL/6N mice, and KC7F2 was used to reduce HIF-1α expression in C57BL/6N mice. Western blot was used to detect the expression of collagen type 1 alpha 1(COL1A1), α-smooth muscle actin (α-SMA), SMAD family member (SAMD) 3, Phospho-SMAD3 (PSMAD3), and HIF-1α. PCR was used to detect the expression of COL1A1, α-SMA, and HIF-1α. Immunohistochemistry was used to detect the expression of COL1A1 and HIF-1α.
resultsIn vitro, compared to the control group, COL1A1, α-SMA, PSMAD3, and HIF-1α expression were elevated in the DMOG group, and COL1A1, α-SMA, PSMAD3, and HIF-1α expression were decreased in the KC7F2 group and siRNA group. Compared to the DMOG group, COL1A1, α-SMA, and PSMAD3 expression were decreased in the DMOG + SIS3 group. In vivo, compared to the saline group, COL1A1, α-SMA, PSMAD3, and HIF-1α expression were increased in the pulmonary tissue of C57BL/6N mice in the silica group. Compared to the silica group, COL1A1, α-SMA, PSMAD3, and HIF-1α expression and the degree of PF were decreased in the silica + KC7F2 group.
conclusionInhibition of HIF-1α reduced α-SMA, decreased COL1A1 expression, and attenuated the degree of PF in C57BL/6N mice. Therefore, HIF-1α may be a new target for the treatment of silica-induced PF.
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