ArticleJournal of orthopaedic surgery and research2020
BNIP3 decreases the LPS-induced inflammation and apoptosis of chondrocytes by promoting the development of autophagy.
Article in Journal of orthopaedic surgery and research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 28 citations in OpenAlex.
- Hsa_circ_0101645 contributes to excessive autophagy and apoptosis in intervertebral disc degeneration by acting as a miR-1304-5p sponge modulating BNIP3 expression.Non-coding RNA research · 2026Article
- BNIP3 induced by hypoxia supports the survival of mesenchymal stromal cells (MSCs) after intravenous cell transplantation.Regenerative therapy · 2025Article
- Mitochondrial Dysfunction in Apoptosis-Resistant Acute Myeloid Leukemia Cells During a Sterile Inflammatory Response.Biomolecules · 2025Article
- Nicotine Attenuates Chondrocyte Inflammation via the α7nAChR-Mediated Inhibition of the HMGB1/TLR4/NF-κB Signaling Pathway.Journal of inflammation research · 2025Article
- The Role of BNIP3 and Blocked Autophagy Flux in Arsenic-Induced Oxidative Stress-Induced Liver Injury in Rats.Biological trace element research · 2024Article
- Mitochondrial mechanisms in the pathogenesis of chronic inflammatory musculoskeletal disorders.Cell & bioscience · 2024Review
- Advances in the study of mitophagy in osteoarthritis.Journal of Zhejiang University. Science. B · 2024Article
- Biomarkers for Diagnosing and Treating Fetal Growth Restriction.Current medicinal chemistry · 2024Review
- Pyroptosis in Osteoarthritis: Molecular Mechanisms and Therapeutic Implications.Journal of inflammation research · 2024Review
- Resveratrol inhibits LPS-induced apoptosis in bovine mammary epithelial cells: the role of PGC1α-SIRT3 axis.In vitro cellular & developmental biology. Animal · 2023Article
- New insights into the interplay between autophagy and oxidative and endoplasmic reticulum stress in neuronal cell death and survival.Frontiers in cell and developmental biology · 2022Review
- Dexmedetomidine Attenuates LPS-Stimulated Alveolar Type II Cells' Injury through Upregulation of miR-140-3p and Partial Suppression of PD-L1 Involving Inactivating JNK-Bnip3 Pathway.Canadian respiratory journal · 2022Article
- Hydroxysafflor Yellow A (HSYA) Protects Endplate Chondrocytes Against IL-1Evidence-based complementary and alternative medicine : eCAM · 2022Article
- BNIP3L/NIX-mediated mitophagy: molecular mechanisms and implications for human disease.Cell death & disease · 2021Review
- Significances of viable synergistic autophagy-associated cathepsin B and cathepsin D (CTSB/CTSD) as potential biomarkers for sudden cardiac death.BMC cardiovascular disorders · 2021Article
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5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInflammation and apoptosis of chondrocytes are the pathological bases of osteoarthritis. Autophagy could alleviate the symptoms of inflammation and apoptosis. Previous study has shown that BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3) can induce the occurrence and development of autophagy. However, it is unknown whether autophagy induced by BNIP3 can alleviate the inflammation and apoptosis of chondrocytes.
methodsWe used the lentivirus to construct the overexpression BNIP3 chondrocytes. Next, the lipopolysaccharide (LPS) was used to stimulate these cells to simulate the physiological environment of osteoarthritis. After that, the enzyme-linked immunosorbent assays (ELISA) were performed to determine the levels of tumor necrosis factor-α (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6) and the flow cytometry was performed to detect the apoptosis rates of chondrocytes. At last, the expression of autophagy-related proteins was detected with the western blotting.
resultsThe expression of BNIP3 was suppressed after treatment with LPS. However, overexpression of BNIP3 inhibited the secretion of proinflammatory factors (TNF-α, IL-1β, and IL-6) and decreased the apoptosis of chondrocytes. Furthermore, overexpression of BNIP3 led to the upregulation of autophagy-related protein expression including little computer 3 (LC3), autophagy-related protein 7 (ATG7), and Beclin-1. Application of autophagy inhibitor recovered the expression of proinflammatory factors and apoptosis rates of chondrocytes.
conclusionsBNIP3 decreased the LPS-induced inflammation and apoptosis of chondrocytes by activating the autophagy.
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