ReviewApoptosis : an international journal on programmed cell death2026
Programmed cell death in osteoarthritis.
Review in Apoptosis : an international journal on programmed cell death, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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
11 citing papers in PubMed.
- Mechanistic insights and therapeutic implications of mitoxyperilysis: a spatially gated mitochondria-dependent lytic cell death.Apoptosis : an international journal on programmed cell death · 2026Review
- Integrated bulk and single-cell transcriptomic analyses and experimental validation reveal the pathogenic role of chondrocyte pyroptosis in osteoarthritis and the therapeutic potential of curcumin via its targeted modulation.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Endocrine‑metabolic imbalance drives osteoarthritis: From whole‑joint pathobiology to precision therapy (Review).International journal of molecular medicine · 2026Review
- RNA cytosine modifications regulates musculoskeletal disorders.Molecular biology reports · 2026Review
- The vicious cycle from inflammation to pyroptosis: the core role of macrophage polarization imbalance in the pathogenesis of knee osteoarthritis.Molecular biology reports · 2026Review
- Research Progress of Cuproptosis in Orthopaedics: Opportunities and Challenges.Journal of cellular and molecular medicine · 2026Review
- TCF4 contributes to OA progression by regulating the transcription of LOXL1.Journal of inflammation (London, England) · 2026Article
- TRIM62 promotes osteoarthritis progression by facilitating GPX4 ubiquitination and chondrocyte ferroptosis.American journal of translational research · 2026Article
- From cartilage degeneration to pain sensitization: a multi-tissue mitochondrial dysfunction network in osteoarthritis.Frontiers in cell and developmental biology · 2026Review
- HIF-1α expression is associated to cell proliferation and ECM production in temporomandibular joint osteoarthritis.PloS one · 2026Article
- Lactate-driven lactylation reprograms chondrocyte fate and joint inflammation in osteoarthritis: linking metabolism with epigenetic regulation.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Osteoarthritis (OA) is a prevalent degenerative joint disease with complex and multifactorial etiology, primarily affecting elderly populations. Factors such as mechanical stress and aging contribute to cartilage degeneration and joint damage. OA manifests through extracellular matrix (ECM) degradation in chondrocytes, decreased chondrocyte viability, and is associated with significant incidence and disability. Recent research indicates that multiple patterns of programmed cell death (PCD), including apoptosis, pyroptosis, necroptosis, autophagy, ferroptosis, cuproptosis, and PANoptosis, regulate the survival and death of chondrocytes through intricate molecular networks, thereby contributing to the onset and progression of OA.This review elucidates the molecular underpinnings of these seven forms of PCD and emphasizes their significance in OA pathology, with a view to providing new perspectives for in-depth research into the pathogenesis of OA and the development of targeted drugs.
Indexed as
Identifiers
41511581What 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.