ArticleJournal of translational medicine2024
Klf10 is involved in extracellular matrix calcification of chondrocytes alleviating chondrocyte senescence.
Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Osteoarthritis: molecular pathogenesis and potential therapeutic options.Signal transduction and targeted therapy · 2026Review
- The gut‑bone‑cartilage triad: Microbial regulation of the Wnt/β‑catenin signaling pathway in osteoarthritis joint remodeling (Review).Molecular medicine reports · 2026Review
- Serum miR-576-5p as a novel diagnostic biomarker and therapeutic target for osteoarthritis via targeting KLF10-mediated chondrocyte dysfunction.BMC musculoskeletal disorders · 2025Article
- Establishment of a medial arterial calcification model in C57BL/6J mice via arterial intimal injury.Cardiovascular diagnosis and therapy · 2025Article
- Extracellular matrix dysregulation in aging, calcification, and cancer diseases: insights into cellular senescence, inflammation, and novel therapeutic strategies.International journal of biological sciences · 2025Review
- CPP-calcification of articular cartilage is associated with elevated cytokine levels in synovial fluid.Frontiers in cell and developmental biology · 2025Article
- Article
- Identification of key biomarkers related to fibrocartilage chondrocytes for osteoarthritis based on bulk, single-cell transcriptomic data.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Osteoarthritis (OA) is a chronic degenerative disease resulting joint disability and pain. Accumulating evidences suggest that chondrocyte extracellular matrix calcification plays an important role in the development of OA. Here, we showed that Krüppel-like factor 10 (Klf10) was involved in the regulation of chondrocyte extracellular matrix calcification by regulating the expression of Frizzled9. Knockdown of Klf10 attenuated TBHP induced calcification and reduced calcium content in chondrocytes. Restoring extracellular matrix calcification of chondrocytes could aggravate chondrocyte senescence. Destabilization of a medial meniscus (DMM) mouse model of OA, in vivo experiments revealed that knockdown Klf10 improved the calcification of articular cartilage and ameliorated articular cartilage degeneration. These findings suggested that knockdown Klf10 inhibited extracellular matrix calcification-related changes in chondrocytes and alleviated chondrocyte senescence.
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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.