The transcription factor JUN is a major regulator of quiescent pancreatic stellate cell maintenance

Lin, Hao; Zheng, Yi; Xu, Rong; Li, Xing-Er; Sun, Bo

doi:10.1016/j.gene.2022.147000

Cited by 1 publication

(1 citation statement)

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“…Regulation of human Reg gene expression could become a key element in future CP therapy [148]. The transcription factor JUN is crucial for maintaining the quiescent state of PSCs, providing a theoretical foundation for the treatment of various pancreatic injuries caused by PSCs [149].…”

Section: Reg1-3mentioning

confidence: 99%

Activation and Regulation of Pancreatic Stellate Cells in Chronic Pancreatic Fibrosis: A Potential Therapeutic Approach for Chronic Pancreatitis

Kong,

Pan,

2024

Biomedicines

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In the complex progression of fibrosis in chronic pancreatitis, pancreatic stellate cells (PSCs) emerge as central figures. These cells, initially in a dormant state characterized by the storage of vitamin A lipid droplets within the chronic pancreatitis microenvironment, undergo a profound transformation into an activated state, typified by the secretion of an abundant extracellular matrix, including α-smooth muscle actin (α-SMA). This review delves into the myriad factors that trigger PSC activation within the context of chronic pancreatitis. These factors encompass alcohol, cigarette smoke, hyperglycemia, mechanical stress, acinar cell injury, and inflammatory cells, with a focus on elucidating their underlying mechanisms. Additionally, we explore the regulatory factors that play significant roles during PSC activation, such as TGF-β, CTGF, IL-10, PDGF, among others. The investigation into these regulatory factors and pathways involved in PSC activation holds promise in identifying potential therapeutic targets for ameliorating fibrosis in chronic pancreatitis. We provide a summary of recent research findings pertaining to the modulation of PSC activation, covering essential genes and innovative regulatory mediators designed to counteract PSC activation. We anticipate that this research will stimulate further insights into PSC activation and the mechanisms of pancreatic fibrosis, ultimately leading to the discovery of groundbreaking therapies targeting cellular and molecular responses within these processes.

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Section: Reg1-3mentioning

confidence: 99%