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Updated: Sep 27, 2025

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
CHD7 regulates bone-fat balance by suppressing PPAR-γ signaling
Caojie Liu1, Qiuchan Xiong1, Qiwen Li1
1State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, PR China.
Chromodomain helicase DNA-binding protein 7 (CHD7) deficiency in bone marrow stem cells causes low bone mass and high marrow fat. Loss of CHD7 disrupts epigenetic regulation of adipogenesis, impacting skeletal health.
Area of Science:
- Molecular Biology
- Genetics
- Developmental Biology
Background:
- Chromodomain helicase DNA-binding protein 7 (CHD7) is crucial for organ development and its mutation causes CHARGE syndrome.
- The role of CHD7 in skeletal development and its underlying mechanisms are not fully understood.
Purpose of the Study:
- To investigate the function and epigenetic mechanisms of CHD7 in skeletal homeostasis.
- To elucidate the impact of CHD7 deficiency on bone marrow mesenchymal stem cells (MSCs) and their differentiation.
Main Methods:
- Conditional knockout of Chd7 in mouse bone marrow MSCs and preosteoblasts.
- Analysis of bone mass, marrow adiposity, and gene expression.
- Investigation of peroxisome proliferator-activated receptor (PPAR) signaling pathway and epigenetic modifications.
Main Results:
- Chd7 knockout in MSCs resulted in significantly reduced bone mass and increased marrow adiposity.
- Loss of CHD7 enhanced PPAR signaling, leading to increased PPAR-γ activity.
- PPAR-γ associated with H3K4me3, activating adipogenic genes and disrupting the osteogenic/adipogenic balance.
Conclusions:
- CHD7 plays a critical role in maintaining skeletal health by regulating MSC differentiation.
- Epigenetic dysregulation of PPAR signaling due to CHD7 loss contributes to skeletal pathologies.
- Findings reveal a novel epigenetic mechanism linking CHD7 to skeletal diseases.
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