Premium
Deficient primary cilia in obese adipose‐derived mesenchymal stem cells: obesity, a secondary ciliopathy?
Author(s) -
Ritter A.,
Louwen F.,
Yuan J.
Publication year - 2018
Publication title -
obesity reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.845
H-Index - 162
eISSN - 1467-789X
pISSN - 1467-7881
DOI - 10.1111/obr.12716
Subject(s) - ciliopathy , cilium , adipose tissue , mesenchymal stem cell , stem cell , microbiology and biotechnology , biology , context (archaeology) , lipotoxicity , inflammation , medicine , endocrinology , insulin resistance , obesity , phenotype , genetics , paleontology , gene
Summary Obesity alters the composition, structure and function of adipose tissue, characterized by chronic inflammation, insulin resistance and metabolic dysfunction. Adipose‐derived mesenchymal stem cells (ASCs) are responsible for cell renewal, spontaneous repair and immunomodulation in adipose tissue. Increasing evidence highlights that ASCs are deficient in obesity, and the underlying mechanisms are not well understood. We have recently shown that obese ASCs have defective primary cilia, which are shortened and unable to properly respond to stimuli. Impaired cilia compromise ASC functions. This work suggests an intertwined connection of obesity, defective cilia and dysfunctional ASCs. We have here discussed the current data regarding defective cilia in various cell types in obesity. Based on these observations, we hypothesize that obesity, a systemic chronic metainflammation, could impair cilia in diverse ciliated cells, like pancreatic islet cells, stem cells and hypothalamic neurons, making these critical cells dysfunctional by shutting down their signal sensors and transducers. In this context, obesity may represent a secondary form of ciliopathy induced by obesity‐related inflammation and metabolic dysfunction. Reactivation of ciliated cells might be an alternative strategy to combat obesity and its associated diseases.