ArticleCell death & disease2018
TFEB, a potential therapeutic target for osteoarthritis via autophagy regulation.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 89 citations in OpenAlex.
- Chondrocyte Senescence in Osteoarthritis: Potential Targets and Pharmacological Interventions.Cartilage · 2026Article
- A therapeutic-grade purified exosome system alleviates osteoarthritis by regulating autophagy through the BCL2-Beclin1 axis.Journal of nanobiotechnology · 2025Article
- The Influence of Sirtuin 6 on Chondrocyte Senescence in Osteoarthritis Under Aging: Focusing on Mitochondrial Dysfunction and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2025Review
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength.JCI insight · 2025Article
- Targeting PNPO to suppress tumor growth via inhibiting autophagic flux and to reverse paclitaxel resistance in ovarian cancer.Apoptosis : an international journal on programmed cell death · 2024Article
- Estrogen receptor is involved in the osteoarthritis mediated by Atg16L1-NLRP3 activation.Joint diseases and related surgery · 2024Article
- Advances in SIRT3 involvement in regulating autophagy-related mechanisms.Cell division · 2024Review
- Lysosomes in senescence and aging.EMBO reports · 2023Review
- Psoralen synergizes with exosome-loaded SPC25 to alleviate senescence of nucleus pulposus cells in intervertebral disc degeneration.Journal of orthopaedic surgery and research · 2023Article
- Ajugol's upregulation of TFEB-mediated autophagy alleviates endoplasmic reticulum stress in chondrocytes and retards osteoarthritis progression in a mouse model.Chinese medicine · 2023Article
- The role of apoptosis in the pathogenesis of osteoarthritis.International orthopaedics · 2023Review
- Autophagy and apoptosis: regulatory factors of chondrocyte phenotype transition in osteoarthritis.Human cell · 2023Review
- Article
- MiR-760 targets HBEGF to control cartilage extracellular matrix degradation in osteoarthritis.Journal of orthopaedic surgery and research · 2023Article
- Transcription factor EB as a key molecular factor in human health and its implication in diseases.SAGE open medicine · 2023Review
- Autophagy in the pathogenesis and therapeutic potential of post-traumatic osteoarthritis.Burns & trauma · 2023Review
- Long intergenic non-protein coding RNA 00707 regulates chondrocyte apoptosis and proliferation in osteoarthritis by serving as a sponge for microRNA-199-3p.Bioengineered · 2022Article
- Blockade of ASIC1a inhibits acid-induced rat articular chondrocyte senescence through regulation of autophagy.Human cell · 2022Article
- New insights into the interplay between autophagy and cartilage degeneration in osteoarthritis.Frontiers in cell and developmental biology · 2022Review
- Loss of Autophagy Causes Increased Apoptosis of Tibial Plateau Chondrocytes in Guinea Pigs with Spontaneous Osteoarthritis.Cartilage · 2021Article
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The blockage of autophagic flux in chondrocytes has been considered as a major reason for the excessive cellular apoptosis and senescence in osteoarthritis (OA) development; however, the molecular mechanism and therapeutic strategy for interrupted autophagic flux is still not clear. Most recently, the transcription factor EB (TFEB) is identified as a master regulator for autophagic flux via initiating the expression of multiple autophagy-related genes and lysosomal biogenesis. This research was performed to confirm whether TFEB expression and activity are impacted in OA development and to confirm the effect of genetic up-regulation of TFEB on autophagic flux and cellular protection in the in vitro and in vivo models of OA. We demonstrated that the expression and nuclear localization of TFEB is decreased in human and mouse OA cartilage as well as in tert-Butyl hydroperoxide (TBHP)-treated chondrocytes. Applying lentivirus to transfect chondrocytes, we found that TFEB overexpression rescues the TBHP-induced the autophagic flux damage, lysosome dysfunction and protects chondrocyte against TBHP induced apoptosis and senescence; these protections of TFEB are diminished by chloroquine-medicated autophagy inhibition. Our destabilized medial meniscus (DMM) mouse OA model shows that TFEB overexpression ameliorates the surgery-induced cartilage degradation, restrains the apoptosis and senescence of chondrocyte, and enhances the autophagic flux. In summary, our study indicates that the activity of TFEB in chondrocyte is involved in OA development, also TFEB overexpression may be a promising strategy for OA treatment.
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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.