Krüppel-like factor 10 (KLF10) as a critical signaling mediator: Versatile functions in physiological and pathophysiological processes

Hong-Yang Luo; Jie-Ying Zhu; Min Chen; Wang-Jing Mu; Liang Guo

doi:10.1016/j.gendis.2022.06.005

Krüppel-like factor 10 (KLF10) as a critical signaling mediator: Versatile functions in physiological and pathophysiological processes

Genes Dis. 2022 Jul 4;10(3):915-930. doi: 10.1016/j.gendis.2022.06.005. eCollection 2023 May.

Authors

Hong-Yang Luo^{1

2}, Jie-Ying Zhu^{1

2}, Min Chen^{1

2}, Wang-Jing Mu^{1

2}, Liang Guo^{1

2}

Affiliations

¹ Shanghai Frontiers Science Research Base of Exercise and Metabolic Health, Shanghai University of Sport, Shanghai 200438, China.
² School of Kinesiology, Shanghai University of Sport, Shanghai 200438, China.

Abstract

Krüppel-like factor 10 (KLF10), also known as TGFβ-inducible early gene-1 (TIEG1), was first found in human osteoblasts. Early studies show that KLF10 plays an important role in osteogenic differentiation. Through decades of research, KLF10 has been found to have complex functions in many different cell types, and its expression and function is regulated in multiple ways. As a downstream factor of transforming growth factor β (TGFβ)/SMAD signaling, KLF10 is involved in various biological functions, including glucose and lipid metabolism in liver and adipose tissue, the maintenance of mitochondrial structure and function of the skeletal muscle, cell proliferation and apoptosis, and plays roles in multiple disease processes, such as nonalcoholic steatohepatitis (NASH) and tumor. Besides, KLF10 shows gender-dependent difference of regulation and function in many aspects. In this review, the biological functions of KLF10 and its roles in disease states is updated and discussed, which would provide new insights into the functional roles of KLF10 and a clearer view of potential therapeutic strategies by targeting KLF10.

Keywords: Adipose tissue; Estrogen signaling; Glucose and lipid metabolism; NASH; Obesity; Skeletal muscle; TGFβ/SMAD signaling; Tumor.

Publication types

Review