Electroacupuncture activates angiogenesis by regulating the PI3K/Pten/Thbs1 signaling pathway to promote the browning of adipose tissue in HFD-induced obese mice

Gao, Hongyan; Li, Yanhui; Jin, Yue; Zhang, Li; Xia, Xiuwen; Liu, Jinkun; Wang, Huaifu; Xie, Ya; Ding, Weijun

doi:10.1016/j.biopha.2023.115386

Cited by 1 publication

(1 citation statement)

References 35 publications

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“…As a classical collagen protein, overexpression of COL4A3 has been extensively implicated in fibrosis (Unamuno et al, 2021) and NAFLD in zebrafish (Forn-Cuní et al, 2015). Elevated THBS1 levels are positively correlated with TG and CHO levels (Gao et al, 2023), as well as liver steatosis grades (Bai et al, 2020). Additionally, increased THBS1 expression has been linked to the activation of epithelial mesenchymal transition (Murphy-Ullrich & Suto, 2018), collagen fibril formation (Rosini et al, 2018), fibroblast migration and activation (Lu et al, 2011), and invasion and migration of gastric cancer cells via the PI3K/AKT/mTOR pathway (Lin et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of wild-type HRAS drives non-alcoholic steatohepatitis to hepatocellular carcinoma in mice

Ling,

Liu,

Wang

et al. 2024

Zoological Research

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Hepatocellular carcinoma (HCC), a prevalent solid carcinoma of significant concern, is an aggressive and often fatal disease with increasing global incidence rates and poor therapeutic outcomes. The etiology and pathological progression of non-alcoholic steatohepatitis (NASH)-related HCC is multifactorial and multistage. However, no single animal model can accurately mimic the full NASH-related HCC pathological progression, posing considerable challenges to transition and mechanistic studies. Herein, a novel conditional inducible wild-type human HRAS overexpressed mouse model (HRAS-HCC) was established, demonstrating 100% morbidity and mortality within approximately one month under normal dietary and lifestyle conditions. Advanced symptoms of HCC such as ascites, thrombus, internal hemorrhage, jaundice, and lung metastasis were successfully replicated in mice. In-depth pathological features of NASH-related HCC were demonstrated by pathological staining, biochemical analyses, and typical marker gene detections. Combined murine anti-PD-1 and sorafenib treatment effectively prolonged mouse survival, further confirming the accuracy and reliability of the model. Based on proteinprotein interaction (PPI) network and RNA sequencing analyses, we speculated that overexpression of HRAS may initiate the THBS1-COL4A3 axis to induce NASH with severe fibrosis, with subsequent progression to HCC.Collectively, our study successfully duplicated natural sequential progression in a single murine model over a very short period, providing an accurate and reliable preclinical tool for therapeutic evaluations targeting the NASH to HCC continuum.

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