ArticleNaunyn-Schmiedeberg's archives of pharmacology2023
Naringin regulates endoplasmic reticulum stress and mitophagy through the ATF3/PINK1 signaling axis to alleviate pulmonary fibrosis.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- Organelle Crosstalk and Metabolic Reprogramming in Idiopathic Pulmonary Fibrosis: Mechanisms and Therapeutic Implications.Cell biochemistry and function · 2026Review
- The protective effects of naringin against cisplatin-induced pulmonary toxicity in rats: Insights into the modulation of ER stress and SIRT1/Nrf2 pathway.BMC complementary medicine and therapies · 2026Article
- Mitophagy in idiopathic pulmonary fibrosis: from molecular mechanisms to therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Naringin mitigates liver damage in a tissue-engineered liver of metabolic dysfunction-associated steatotic liver disease model by promoting autophagy via the mTOR-ULK1 pathway.Molecular biology reports · 2025Article
- Double-edged mitophagy: balancing inflammation and resolution in lung disease.Clinical science (London, England : 1979) · 2025Review
- Modulating NLRP3 Inflammasomes in Idiopathic Pulmonary Fibrosis: A Comprehensive Review on Flavonoid-Based Interventions.Cell biochemistry and biophysics · 2025Review
- ATF3 Knockdown Exacerbates Astrocyte Activation by Inhibiting Phosphorylation of Drp1 in Ischemic Stroke.Biologics : targets & therapy · 2025Article
- Hydrogen improves the efficacy of tetrandrine in the treatment of silicosis by inhibiting vascular endothelial mesenchymal transition caused by oxidative stress.Frontiers in bioengineering and biotechnology · 2025Article
- Mitochondrial dysfunction and alveolar type II epithelial cell senescence: The destroyer and rescuer of idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2025Review
- Curculigoside Attenuates Endoplasmic Reticulum Stress-Induced Epithelial Cell and Fibroblast Senescence by Regulating the SIRT1-P300 Signaling Pathway.Antioxidants (Basel, Switzerland) · 2024Article
- Review
- Potential Beneficial Effects of Naringin and Naringenin on Long COVID-A Review of the Literature.Microorganisms · 2024Review
- The Dual Roles of Activating Transcription Factor 3 (ATF3) in Inflammation, Apoptosis, Ferroptosis, and Pathogen Infection Responses.International journal of molecular sciences · 2024Review
- Effects of Natural Products through Inhibiting Endoplasmic Reticulum Stress on Attenuation of Idiopathic Pulmonary Fibrosis.Drug design, development and therapy · 2024Review
- Understanding the molecular regulatory mechanisms of autophagy in lung disease pathogenesis.Frontiers in immunology · 2024Review
- Mitophagy in fibrotic diseases: molecular mechanisms and therapeutic applications.Frontiers in physiology · 2024Review
- Natural plant resource flavonoids as potential therapeutic drugs for pulmonary fibrosis.Heliyon · 2023Review
- Naringenin ameliorates cytotoxic effects of bisphenol A on mouse Sertoli cells by suppressing oxidative stress and modulating mitophagy: An experimental study.International journal of reproductive biomedicine · 2023Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease that is characterized by abnormal proliferation of fibroblasts and extracellular matrix remodeling, ultimately leading to respiratory insufficiency or even death. Naringin (Nar), a natural compound derived from grapefruit and citrus fruits, has several pharmacological activities that are associated with therapeutic benefits for IPF. However, the specific molecular mechanisms underlying its pulmonary tissue-protective effects remain largely unknown. This study aimed to investigate the effects of Nar on endoplasmic reticulum stress (ERS) and mitophagy. A bleomycin (BLM)-induced mouse model of IPF was established for treatment with different doses of Nar. Histopathological changes in the lung were examined by hematoxylin and eosin (HE) staining and Masson staining. The extent of fibrosis was determined by measuring hydroxyproline and collagen expression levels. The levels of inflammatory cytokines and oxidative stress indicators were determined by Enzyme linked immunosorbent assay (ELISA) and biochemical kits. Western blot and immunofluorescence were used to evaluate the expression levels of the mitophagy-related markers. Cell apoptosis was estimated by western blot and TUNEL staining. Nar reduced the levels of inflammatory response, oxidative stress and decreased the proportion of apoptosis. Nar also inhibited the expression of the ERS and mitophagy-related genes and ERS-downstream proteins, thereby activating transcription factor (ATF) 3 and inhibiting the transcription of PTEN-induced kinase 1 (PINK1). Taken together, Nar is a promising therapeutic agent for treating IPF via inhibiting ERS, reducing apoptosis, and maintaining mitochondrial homeostasis, all of which may be associated with the regulation of the ATF3/PINK1 signaling axis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.