ArticleMolecular medicine (Cambridge, Mass.)2020
Conditional deletion of HDAC4 from collagen type 2α1-expressing cells increases angiogenesis in vivo.
Article in Molecular medicine (Cambridge, Mass.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 8 citations in OpenAlex.
- LMK-235 suppresses osteoclastogenesis and promotes osteoblastogenesis by inhibiting HDAC4.Scientific reports · 2024Article
- FTY720 Attenuates LPS-Induced Inflammatory Bone Loss by Inhibiting Osteoclastogenesis via the NF-Journal of immunology research · 2023Article
- The Status Quo of College Students' Participation in English Online Learning in the Blended Learning Environment and the Ways to Improve It.Journal of environmental and public health · 2022Article
- Article
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Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundHDAC4 is a key regulator of chondrocyte hypertrophy and skeletal development, but it is not clear whether the increase in vascular invasion at growth plates is related to HDAC4 expression. To determine it, we investigated the relationship between HDAC4 and angiogenesis in both in vivo and in vitro models.
methodsHDAC4 was deleted in Col2α1-Cre; HDAC4
resultsThe Col2α1-Cre; HDAC4
conclusionsHDAC4 expression in chondrocytes contributes to angiogenesis in the growth plate, and its absence in vivo negatively affects growth plates.
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