ArticleCells2021
BNIP3-Dependent Mitophagy via PGC1α Promotes Cartilage Degradation.
Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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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
35 citing papers in PubMed, 50 citations in OpenAlex.
- Programmed cell death in osteoarthritis.Apoptosis : an international journal on programmed cell death · 2026Review
- Host miRNA orchestration of mitophagy pathways during bacterial infection: current advances and future directions.Frontiers in microbiology · 2026Review
- Traditional Chinese medicine-derived monomers protect chondrocytes and delay osteoarthritis progression by regulating mitochondrial quality control.Frontiers in molecular biosciences · 2026Review
- Mechanism driven adaptation of smart hydrogels to the osteoarthritis pathological microenvironment.Frontiers in bioengineering and biotechnology · 2026Review
- Multiple strategies, one mission: mesenchymal stromal cell-based mechanisms of action in osteoarthritis.Frontiers in cell and developmental biology · 2026Review
- Adipose-derived mesenchymal stem cell therapy modulates mitochondrial function to attenuate acetaminophen-induced liver injury by DDIT4/PGC-1α axis.Stem cell research & therapy · 2025Article
- The impact of mitochondrial dysfunction on osteoarthritis cartilage: current insights and emerging mitochondria-targeted therapies.Bone research · 2025Review
- Zileuton Attenuates Acute Kidney Injury in Glycerol-Induced Rhabdomyolysis by Regulating Myeloid-Derived Suppressor Cells in Mice.International journal of molecular sciences · 2025Article
- Regulation of RPE65 expression in human retinal pigment epithelium cells.Scientific reports · 2025Article
- A Molecular Chemical Perspective: Mitochondrial Dynamics Is Not a Bystander of Cartilage Diseases.ACS pharmacology & translational science · 2025Review
- Fasting activates optineurin-mediated mitophagy in chondrocytes to protect against osteoarthritis.Communications biology · 2025Article
- Recent development of mitochondrial metabolism and dysfunction in osteoarthritis.Frontiers in pharmacology · 2025Review
- Innovative Biotherapies and Nanotechnology in Osteoarthritis: Advancements in Inflammation Control and Cartilage Regeneration.International journal of molecular sciences · 2024Review
- Feasibility and Safety of Targeting Mitochondria Function and Metabolism in Acute Myeloid Leukemia.Current pharmacology reports · 2024Article
- From dysfunction to healing: advances in mitochondrial therapy for Osteoarthritis.Journal of translational medicine · 2024Review
- Targeting Parkin-regulated metabolomic change in cartilage in the treatment of osteoarthritis.iScience · 2024Article
- The role and intervention of mitochondrial metabolism in osteoarthritis.Molecular and cellular biochemistry · 2024Review
- Prognositic value of anoikis and tumor immune microenvironment-related gene in the treatment of osteosarcoma.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Article
- Advances in the study of mitophagy in osteoarthritis.Journal of Zhejiang University. Science. B · 2024Article
- Epigenetics in Knee Osteoarthritis: A 2020-2023 Update Systematic Review.Life (Basel, Switzerland) · 2024Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Since mitochondria are suggested to be important regulators in maintaining cartilage homeostasis, turnover of mitochondria through mitochondrial biogenesis and mitochondrial degradation may play an important role in the pathogenesis of osteoarthritis (OA). Here, we found that mitochondrial dysfunction is closely associated with OA pathogenesis and identified the peroxisome proliferator-activated receptor-gamma co-activator 1-alpha (PGC1α) as a potent regulator. The expression level of PGC1α was significantly decreased under OA conditions, and knockdown of PGC1α dramatically elevated the cartilage degradation by upregulating cartilage degrading enzymes and apoptotic cell death. Interestingly, the knockdown of PGC1α activated the parkin RBR E3 ubiquitin protein ligase (PRKN)-independent selective mitochondria autophagy (mitophagy) pathway through the upregulation of BCL2 and adenovirus E1B 19-kDa-interacting protein 3 (BNIP3). The overexpression of BNIP3 stimulated mitophagy and cartilage degradation by upregulating cartilage-degrading enzymes and chondrocyte death. We identified microRNA (miR)-126-5p as an upstream regulator for PGC1α and confirmed the direct binding between miR-126-5p and 3' untranslated region (UTR) of PGC1α. An in vivo OA mouse model induced by the destabilization of medial meniscus (DMM) surgery, and the delivery of antago-miR-126 via intra-articular injection significantly decreased cartilage degradation. In sum, the loss of PGC1α in chondrocytes due to upregulation of miR-126-5p during OA pathogenesis resulted in the activation of PRKN-independent mitophagy through the upregulation of BNIP3 and stimulated cartilage degradation and apoptotic death of chondrocytes. Therefore, the regulation of PGC1α:BNIP3 mitophagy axis could be of therapeutic benefit to cartilage-degrading diseases.
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Registered trials
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.