ReviewHuman cell2023
Autophagy and apoptosis: regulatory factors of chondrocyte phenotype transition in osteoarthritis.
Review in Human cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 2 syntheses or guidelines pooled it, 33 citations in OpenAlex.
- Preclinical pharmacological effects of epimedium-derived interventions in osteoarthritis: a systematic review and meta-analysis.Frontiers in pharmacology · 2026Pooled it
- Bibliometric analysis of research trends and emerging insights of osteoarthritis and chondrocyte hypertrophy.Frontiers in surgery · 2025Pooled it
- Single-cell sequencing and machine learning-based prediction of spliceosome-associated factor 2 may represent potential targets for osteoarthritis.Osteoarthritis and cartilage open · 2026Article
- Research Progress of Cuproptosis in Orthopaedics: Opportunities and Challenges.Journal of cellular and molecular medicine · 2026Review
- Research progress of cuproptosis, ferroptosis, apoptosis, and autophagy in knee osteoarthritis.Frontiers in cell and developmental biology · 2026Review
- Senescence-associated secretory phenotype: the "pathogenic" factor driving orthopedic degenerative diseases and its regulation.Frontiers in aging · 2026Review
- Pterostilbene attenuates osteoarthritis progression through p53-dependent autophagy activation: evidence from network analysis and experimental validation.Frontiers in pharmacology · 2026Article
- The Influence of Sirtuin 6 on Chondrocyte Senescence in Osteoarthritis Under Aging: Focusing on Mitochondrial Dysfunction and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2025Review
- Increased Rab1a accelerates osteoarthritis by inhibiting autophagy via activation of the mTORC1-S6K pathway.Journal of advanced research · 2025Article
- Neutralization of acyl CoA binding protein (ACBP) for the experimental treatment of osteoarthritis.Cell death and differentiation · 2025Article
- Exploring the mechanisms of PANoptosis in osteoarthritis and the therapeutic potential of andrographolide through bioinformatics and single-cell analysis.Biology direct · 2025Article
- CircTBCK protects against osteoarthritis by regulating extracellular matrix and autophagy.Human cell · 2025Article
- Mechanosensitive lncRNA H19 promotes chondrocyte autophagy, but not pyroptosis, by targeting miR-148a in post-traumatic osteoarthritis.Non-coding RNA research · 2025Article
- Article
- Artificial Cell-Derived Vesicles: Extracellular Vesicle Mimetics for Chondrocyte Restoration in TMJOA Therapy.International journal of nanomedicine · 2025Article
- Article
- Programmed Cell Death of Chondrocytes, Synovial Cells, Osteoclasts, and Subchondral Bone Cells in Osteoarthritis.Journal of inflammation research · 2025Review
- Immunometabolic regulation of disulfidptosis in orthopedic diseases: mechanistic heterogeneity and therapeutic targets.Frontiers in immunology · 2025Review
- New insights into the mechanisms and therapeutic strategies of chondrocyte autophagy in osteoarthritis.Journal of molecular medicine (Berlin, Germany) · 2024Review
- The role of mitochondrial autophagy in osteoarthritis.iScience · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is the main pathogenic factor in diseases that cause joint deformities. As the main manifestation of the progress of OA, cartilage degradation has been closely associated with the degeneration of chondrocytes, which is induced by inflammatory factors and other trauma factors. Autophagy and apoptosis are the main mechanisms for cells to maintain homeostasis and play crucial roles in OA. Under the influence of external environmental factors (such as aging and injury), the metabolism of cells can be altered, which may affect the extent of autophagy and apoptosis. With the progression of OA, these changes can alter the cell phenotypes, and the cells of different phenotypes display distinct differences in morphology and function. In this review, we have summarized the alteration in cell metabolism, autophagy, and the extent of apoptosis during OA progression and its effects on the cell phenotypes to provide new ideas for further research on the mechanisms of phenotypic transition and therapeutic strategies so as to reverse the cell phenotypes.
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What OpenQuestion holds
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.