ArticleFunctional & integrative genomics2022
Subversive molecular role of Krüppel-like factor 5 in extracellular matrix degradation and chondrocyte dedifferentiation.
Article in Functional & integrative genomics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 8 citations in OpenAlex.
- KLF5 aggravates osteoarthritis progression by inhibiting chondrocyte autophagy via transcriptional activation of PLK2.Scientific reports · 2025Article
- Krüppel-like factors family in health and disease.MedComm · 2024Review
- KLF transcription factors in bone diseases.Journal of cellular and molecular medicine · 2024Review
- Deciphering the RNA-binding protein interaction with the mRNAs encoded from human chromosome 15q11.2 BP1-BP2 microdeletion region.Functional & integrative genomics · 2023Article
- Analysis of the regulatory role of miR-34a-5p/PLCD3 in the progression of osteoarthritis.Functional & integrative genomics · 2023Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Osteoarthritis (OA) is the most common joint disorder worldwide and a leading cause of pain and disability. However, the pathogenesis of osteoarthritis has not been elucidated. Krüppel-like factor (KLF)-5 is involved in several biological processes, including inflammation and cell differentiation, but its role in OA has not been evaluated. In this study, we investigated the role of KLF-5 in chondrocyte differentiation. KLF-5 overexpression in chondrocytes induced a loss of type II collagen expression and sulfated proteoglycan synthesis at the transcriptional and translational levels. Based on immunofluorescence staining, the ectopic expression of KLF-5 reduced type II collagen expression. In contrast, with KLF-5-transfected cells, KLF-5 siRNA transfection-induced type II expression also blocked dedifferentiation caused by the overexpression of KLF-5. In zebra fish, KLF-5 reduced the sulfated proteoglycan synthesis of ceratobranchial cartilage. Our results suggest that KLF-5 plays a pivotal role in the dedifferentiation of rabbit articular cartilage and zebra fish, providing a basis for therapeutic strategy for osteoarthritis aimed at controlling cartilage destruction.
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Registered trials
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