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Peer-reviewedCC BY-NC-NDNature communications

Transient activation of ciliary CCR2 signaling promotes the initiation of adipogenesis.

  • Yue Wu1
  • Yun Kong2
  • Weitao Li1
  • Yanchun Ma1
  • Shaodong Yan1
  • Jun Zhou3,4
  • Yunfan Yang5
5 affiliations
  1. 1Center for Cell Structure and Function, College of Life Sciences, Shandong Normal University, Jinan, China.
  2. 2Department of Cell Biology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, China.
  3. 3Center for Cell Structure and Function, College of Life Sciences, Shandong Normal University, Jinan, China. [email protected].
  4. 4State Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China. [email protected].
  5. 5State Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, Tianjin, China. [email protected].
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Abstract

Despite extensive evidence linking inflammation to obesity, a clear mechanistic model for how inflammatory signals regulate adipose tissue development remains lacking. Here, using in vitro and in vivo models, we demonstrate that transient primary cilium assembly and cilium-dependent inflammatory signaling in preadipocytes serve as key initiators of adipogenesis. Adipose stem cells transiently activate a ciliary gene program to form ciliated preadipocytes, which subsequently commit to adipogenesis and lose their cilia upon further differentiation. We further show that C-C motif chemokine receptor 2 (CCR2) localizes to the primary cilia of preadipocytes. High-fat diet feeding remodels the adipose tissue microenvironment, elevating the pro-inflammatory chemokine C-C motif chemokine ligand 2 (CCL2), which engages the cilium-localized CCR2 to initiate adipogenesis via an extracellular signal-regulated kinase (ERK)-dependent signaling pathway. Disruption of cilium assembly or interference with the downstream CCL2/CCR2-ERK signaling axis severely impairs adipogenesis. These findings reveal that the transient assembly of primary cilia in preadipocytes establishes a temporally confined window of heightened sensitivity to environmental inflammatory cues, directing cell fate decisions in adipose tissue development.

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Cite

BibTeXRIS
BibTeX
@article{wu2026transient,
  title = {{Transient activation of ciliary CCR2 signaling promotes the initiation of adipogenesis.}},
  author = {Yue Wu and Yun Kong and Weitao Li and Yanchun Ma and Shaodong Yan and Jun Zhou and Yunfan Yang},
  journal = {Nature communications},
  year = {2026},
  month = sep,
  doi = {10.1038/s41467-026-77826-0},
  url = {https://europepmc.org/article/MED/42893979},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Transient activation of ciliary CCR2 signaling promotes the initiation of adipogenesis.
AU  - Yue Wu
AU  - Yun Kong
AU  - Weitao Li
AU  - Yanchun Ma
AU  - Shaodong Yan
AU  - Jun Zhou
AU  - Yunfan Yang
PY  - 2026
DA  - 2026/09/17
JO  - Nature communications
DO  - 10.1038/s41467-026-77826-0
UR  - https://europepmc.org/article/MED/42893979
AB  - Despite extensive evidence linking inflammation to obesity, a clear mechanistic model for how inflammatory signals regulate adipose tissue development remains lacking. Here, using in vitro and in vivo models, we demonstrate that transient primary cilium assembly and cilium-dependent inflammatory signaling in preadipocytes serve as key initiators of adipogenesis. Adipose stem cells transiently activate a ciliary gene program to form ciliated preadipocytes, which subsequently commit to adipogenesis and lose their cilia upon further differentiation. We further show that C-C motif chemokine receptor 2 (CCR2) localizes to the primary cilia of preadipocytes. High-fat diet feeding remodels the adipose tissue microenvironment, elevating the pro-inflammatory chemokine C-C motif chemokine ligand 2 (CCL2), which engages the cilium-localized CCR2 to initiate adipogenesis via an extracellular signal-regulated kinase (ERK)-dependent signaling pathway. Disruption of cilium assembly or interference with the downstream CCL2/CCR2-ERK signaling axis severely impairs adipogenesis. These findings reveal that the transient assembly of primary cilia in preadipocytes establishes a temporally confined window of heightened sensitivity to environmental inflammatory cues, directing cell fate decisions in adipose tissue development.
SN  - 2041-1723
ER  -