Acetaminophen-induced reduction of NIMA-related kinase 7 expression exacerbates acute liver injury

Sun, Zhenzhen; Wang, Qian; Sun, Lin; Wu, Mengying; Li, Shuzhen; Hu, Hua; Sun, Ying; Ni, Tong; Zhou, Chunlei; Huang, Songming; Zhang, Aihua; Zhang, Yue

doi:10.1016/j.jhepr.2022.100545

Cited by 11 publications

(6 citation statements)

References 50 publications

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“…After the surgery, the mice were placed on a heating pad for recovering before being transferred back to the cage. In the second model, acetaminophen (PHx) was administered in 8-week male mice as previously described 21 , 22 . Briefly, the mice were fasted overnight (12–16 h) with free access to water.…”

Section: Methodsmentioning

confidence: 99%

Phosphatidic acid-enabled MKL1 contributes to liver regeneration: Translational implication in liver failure

Zhou,

Sun,

Chen

et al. 2024

Acta Pharmaceutica Sinica B

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Section: Methodsmentioning

confidence: 99%

Phosphatidic acid-enabled MKL1 contributes to liver regeneration: Translational implication in liver failure

Zhou,

Sun,

Chen

et al. 2024

Acta Pharmaceutica Sinica B

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“…Partial hepatectomy was performed as previously described [ 21 , 22 ]. Acetaminophen (APAP) was dissolved in 1XPBS and the mice received a single injection at a dose of 300 mg/kg as previously described [ 23 , 24 ]. Plasma LDH levels were measured using a commercially available kit (Abcam, ab102526) per vendor instructions.…”

Section: Methodsmentioning

confidence: 99%

TRIB1 regulates liver regeneration by antagonizing the NRF2-mediated antioxidant response

et al. 2023

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Robust regenerative response post liver injuries facilitates the architectural and functional recovery of the liver. Intrahepatic redox homeostasis plays a key role in liver regeneration. In the present study, we investigated the contributory role of Tribbles homolog 1 (Trib1), a pseudokinase, in liver regeneration and the underlying mechanism. We report that Trib1 expression was transiently down-regulated in animal and cell models of liver regeneration. Further analysis revealed that hepatocyte growth factor (HGF) repressed Trib1 transcription by evicting liver X receptor (LXRα) from the Trib1 promoter. Knockdown of Trib1 enhanced whereas over-expression of Trib1 suppressed liver regeneration after partial hepatectomy in mice. Of interest, regulation of liver regenerative response by Trib1 coincided with alterations of intracellular ROS levels, GSH levels, and antioxidant genes. Transcriptional assays suggested that Trib1 influenced cellular redox status by attenuating nuclear factor erythroid 2-related factor 2 (Nrf2) activity. Mechanistically, Trib1 interacted with the C-terminus of Nrf2 thus masking a potential nuclear localization signal (NLS) and blocking nuclear accumulation of Nrf2. Finally, correlation between Trib1 expression, Nrf2 nuclear localization, and cell proliferation was identified in liver specimens taken from patients with acute liver failure. In conclusion, our data unveil a novel pathway that depicts Trib1 as a critical link between intracellular redox homeostasis and cell proliferation in liver regeneration.

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“…In recent years, increasing evidence has demonstrated that apoptosis plays an important role in APAP-induced liver injury; tune staining has also demonstrated that hepatocytes underwent massive apoptosis in an APAP-induced acute liver injury model in mice [ 123 , 124 ]. Kaempferol (KA), a flavonoid compound extracted from Penthorum chinense, has powerful anti-inflammatory and antioxidant activities.…”

Section: Nlrp3 Inflammasome and Programmed Cell Death In Alimentioning

confidence: 99%

The Role of the NLRP3 Inflammasome and Programmed Cell Death in Acute Liver Injury

Chen

Miao

et al. 2023

IJMS

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Acute liver injury (ALI) is a globally important public health issue that, when severe, rapidly progresses to acute liver failure, seriously compromising the life safety of patients. The pathogenesis of ALI is defined by massive cell death in the liver, which triggers a cascade of immune responses. Studies have shown that the aberrant activation of the nod-like receptor protein 3 (NLRP3) inflammasome plays an important role in various types of ALI and that the activation of the NLRP3 inflammasome causes various types of programmed cell death (PCD), and these cell death effectors can in turn regulate NLRP3 inflammasome activation. This indicates that NLRP3 inflammasome activation is inextricably linked to PCD. In this review, we summarize the role of NLRP3 inflammasome activation and PCD in various types of ALI (APAP, liver ischemia reperfusion, CCl4, alcohol, Con A, and LPS/D-GalN induced ALI) and analyze the underlying mechanisms to provide references for future relevant studies.

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Acetaminophen-induced reduction of NIMA-related kinase 7 expression exacerbates acute liver injury

Cited by 11 publications

References 50 publications

Phosphatidic acid-enabled MKL1 contributes to liver regeneration: Translational implication in liver failure

Phosphatidic acid-enabled MKL1 contributes to liver regeneration: Translational implication in liver failure

TRIB1 regulates liver regeneration by antagonizing the NRF2-mediated antioxidant response

The Role of the NLRP3 Inflammasome and Programmed Cell Death in Acute Liver Injury

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