ArticleConnective tissue research2018
5,7,3',4'-Tetramethoxyflavone protects chondrocytes from ER stress-induced apoptosis through regulation of the IRE1α pathway.
Article in Connective tissue research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- Endoplasmic reticulum stress-mediated apoptosis and autophagy in osteoarthritis: From molecular mechanisms to therapeutic applications.Cell stress & chaperones · 2024Review
- IRE1α pathway: A potential bone metabolism mediator.Cell proliferation · 2024Review
- Hydroxylated Tetramethoxyflavone Affects Intestinal Cell Permeability and Inhibits Cytochrome P450 Enzymes.Molecules (Basel, Switzerland) · 2024Article
- Therapeutic targets and potential delivery systems of melatonin in osteoarthritis.Frontiers in immunology · 2024Review
- The Role of Regulated Programmed Cell Death in Osteoarthritis: From Pathogenesis to Therapy.International journal of molecular sciences · 2023Review
- Protective Effects of Astilbin Against Cadmium-Induced Apoptosis in Chicken Kidneys via Endoplasmic Reticulum Stress Signaling Pathway.Biological trace element research · 2022Article
- Melatonin promotes sirtuin 1 expression and inhibits IRE1α-XBP1S-CHOP to reduce endoplasmic reticulum stress-mediated apoptosis in chondrocytes.Frontiers in pharmacology · 2022Article
- IRE1 signaling regulates chondrocyte apoptosis and death fate in the osteoarthritis.Journal of cellular physiology · 2022Review
- Emerging Natural-Product-Based Treatments for the Management of Osteoarthritis.Antioxidants (Basel, Switzerland) · 2021Review
- Review
- Exploration of the mechanism of tetramethoxyflavone in treating osteoarthritis based on network pharmacology and molecular docking.Tzu chi medical journalArticle
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
aim of the studyTo investigate the roles of endoplasmic reticulum (ER) transmembrane sensor inositol-requiring enzyme-1 (IRE1)α signaling in ER stress-induced chondrocyte apoptosis, and to determine the molecular mechanisms underlying chondroprotective activity of 5,7,3',4'-tetramethoxyflavone (TMF) from Murraya exotica. MATERIALS AND
methodsIRE1α was knocked down by siRNA transfection in chondrocytes, which were harvested from rats' knee cartilages. Chondrocytes with IRE1α deficiency were administrated with tunicamycin (TM) and TMF. Chondrocyte apoptosis was quantified by flow cytometry and DAPI/TUNEL staining. Expression of mRNA and proteins was quantified by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western-blot, respectively.
resultsIRE1α deficiency significantly increased the rate of TM-induced chondrocyte apoptosis, down-regulated the expression of pro-survival factors XBP1S and Bcl-2, and up-regulated pro-apoptotic factors CHOP, p-JNK, and caspase-3. TMF suppressed TM-induced chondrocyte apoptosis by activating the expression of IRE1α, which reversed the expression patterns of downstream pro-survival and pro-apoptotic factors due to IRE1α deficiency.
conclusionThe mechanism of TMF in protecting chondrocytes against ER stress-induced apoptosis might be associated with regulating the activity of ER sensor IRE1α and its downstream pathway.
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Registered trials
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