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Article

Conditional deletion of HDAC4 from collagen type 2α1-expressing cells increases angiogenesis in vivo.

Molecular medicine (Cambridge, Mass.) - 1 May 2020

Gao Lilan, Li Shengchun, Wei Xiaochun, Du Guoqing, Wei Dennis, Wei Lei

Abstract excerpt

BACKGROUND: HDAC4 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. METHODS: HDAC4 was deleted in Col2α1-Cre; HDAC4fl/fl mice. Growth of the Col2α1-Cre; HDAC4d/d...

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Topics

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Share to Chondrocytes
Share to Chondrogenesis
Share to Collagen Type II

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Deletion

Share to Genes, Reporter

Share to Histone Deacetylases

Share to Mice, Transgenic

Share to Neovascularization, Physiologic

Source

Open in PubMed Open full text

Identifiers

PMID: 32354322
DOI: 10.1186/s10020-020-00154-6
PMCID: PMC7193350

Genes

HDAC4
CD34

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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