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<p>The global incidence of obesity-related metabolic disorders and their comorbidities continue to increase along with a demand for innovative therapeutic interventions. An in-depth understanding of de novo thermogenic adipogenesis is vital to harness the potential of these adipocytes. Here, we combine genetic lineage tracing and single-nucleus RNA sequencing to demonstrate that adult adipose-resident c-kit<sup>+</sup> cells are previously unidentified brown adipocyte progenitor cells (APCs). c-kit<sup>+</sup> APCs differentiate into brown adipocytes but not white adipocytes in adipose tissue homeostasis as well as in cold exposure-, high-fat diet (HFD)- and aging-induced adipose remodeling. More importantly, the vital role of c-kit<sup>+</sup> APCs in the generation of brown adipocytes is indicated by decreased brown fat, impaired thermogenic capacity, and excessive fat accumulation in c-kit mutant mice of both genders. In conclusion, the present study demonstrates that adult c-kit<sup>+</sup> APCs give rise to brown adipocytes which are responsible for fat homeostasis and remodeling. Thus, c-kit<sup>+</sup> progenitors may be an innovative and crucial target for obesity and metabolic diseases.</p>

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Commitment of adipose-resident c-kit+ progenitors to brown adipocytes contributes to adipose tissue homeostasis and remodeling

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年7月1日

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  • Qishan Chen,
  • Ya Yu,
  • Run Zhang,
  • Qiaohang Zhao,
  • Danqing Yu,
  • Chun Feng,
  • Jiaojiao Zhou,
  • Meng Luo,
  • Mei Yang,
  • ShaSha Sun,
  • Li Zhang,
  • Min Jin

摘要

The global incidence of obesity-related metabolic disorders and their comorbidities continue to increase along with a demand for innovative therapeutic interventions. An in-depth understanding of de novo thermogenic adipogenesis is vital to harness the potential of these adipocytes. Here, we combine genetic lineage tracing and single-nucleus RNA sequencing to demonstrate that adult adipose-resident c-kit+ cells are previously unidentified brown adipocyte progenitor cells (APCs). c-kit+ APCs differentiate into brown adipocytes but not white adipocytes in adipose tissue homeostasis as well as in cold exposure-, high-fat diet (HFD)- and aging-induced adipose remodeling. More importantly, the vital role of c-kit+ APCs in the generation of brown adipocytes is indicated by decreased brown fat, impaired thermogenic capacity, and excessive fat accumulation in c-kit mutant mice of both genders. In conclusion, the present study demonstrates that adult c-kit+ APCs give rise to brown adipocytes which are responsible for fat homeostasis and remodeling. Thus, c-kit+ progenitors may be an innovative and crucial target for obesity and metabolic diseases.