Role of partial hepatectomy on Capillaria hepatica-induced hepatic fibrosis in rats

Santos, Carolina Cincurá Silva; Onofre-Nunes, Záira; Andrade, Zilton A.

doi:10.1590/s0037-86822007000500001

Cited by 7 publications

(2 citation statements)

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“…Reduced liver regeneration is a feature of liver disease and is correlated with fibrogenesis 6 . Resection of the liver by surgery, also known as partial hepatectomy (PH), triggers regeneration without fibrosis, because the regeneration of hepatic parenchyma outcompetes the growth of fibrous tissue 7 . In a rat model, PH could accelerate the reversion of liver fibrosis through proregeneration 8 .…”

Section: Introductionmentioning

confidence: 99%

“…6 Resection of the liver by surgery, also known as partial hepatectomy (PH), triggers regeneration without fibrosis, because the regeneration of hepatic parenchyma outcompetes the growth of fibrous tissue. 7 In a rat model, PH could accelerate the reversion of liver fibrosis through proregeneration. 8 Likewise, parenchymal cell grafts can also stimulate liver regeneration and reduce fibrosis.…”

Section: Introductionmentioning

confidence: 99%

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Ursodesoxycholic acid alleviates liver fibrosis via proregeneration by activation of the ID1‐WNT2/HGF signaling pathway

Xi¹,

Luo²,

Lu³

et al. 2021

Clinical & Translational Med

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Background The human liver possesses a remarkable capacity for self‐repair. However, liver fibrosis remains a serious medical concern, potentially progressing to end‐stage liver cirrhosis and even death. Liver fibrosis is characterized by excess accumulation of extracellular matrix in response to chronic injury. Liver regenerative ability, a strong indicator of liver health, is important in resisting fibrosis. In this study, we provide evidence that ursodesoxycholic acid (UDCA) can alleviate liver fibrosis by promoting liver regeneration via activation of the ID1‐WNT2/hepatocyte growth factor (HGF) pathway. Methods Bile duct ligation (BDL) and partial hepatectomy (PH) mouse models were used to verify the effects of UDCA on liver fibrosis, regeneration, and the ID1‐WNT2/HGF pathway. An Id1 knockdown mouse model was also used to assess the role of Id1 in UDCA alleviation of liver fibrosis. Results Our results demonstrate that UDCA can alleviate liver fibrosis in the BDL mice and promote liver regeneration via the ID1‐WNT2/HGF pathway in PH mice. In addition, Id1 knockdown abolished the protection afforded by UDCA in BDL mice. Conclusions We conclude that UDCA protects against liver fibrosis by proregeneration via activation of the ID1‐WNT2/HGF pathway.

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Section: Introductionmentioning

confidence: 99%