Adipocytes not only function as energy depots but also secrete numerous
adipokines that regulate multiple metabolic processes, including
lipid homeostasis. Dysregulation of
lipid homeostasis, which often leads to adipocyte
hypertrophy and/or ectopic
lipid deposition in non-adipocyte cells such as muscle and liver, is linked to the development of
insulin resistance. Similarly, an altered secretion profile of
adipokines or imbalance between calorie intake and energy expenditure is associated with
obesity, among other related metabolic disorders. In lungs,
lipid-laden adipocyte-like cells known as lipofibroblasts share numerous developmental and functional similarities with adipocytes, and similarly influence alveolar
lipid homeostasis by facilitating
pulmonary surfactant production. Unsurprisingly, disruption in alveolar
lipid homeostasis may propagate several chronic inflammatory disorders of the lung. Given the numerous similarities between the two cell types, dissecting the molecular mechanisms underlying adipocyte development and function will offer valuable insights that may be applied to, at least, some aspects of lipofibroblast biology in normal and diseased lungs. FGF10, a major
ligand for
FGFR2b, is a multifunctional
growth factor that is indispensable for several biological processes, including development of various organs and tissues such as the lung and WAT. Moreover, accumulating evidence strongly implicates FGF10 in several key aspects of adipogenesis as well as lipofibroblast formation and maintenance, and as a potential player in adipocyte metabolism. This review summarizes our current understanding of the role of FGF10 in adipocytes, while attempting to derive insights on the existing literature and extrapolate the knowledge to pulmonary lipofibroblasts.