Yes-associated protein inhibition ameliorates liver fibrosis and acute and chronic liver failure by decreasing ferroptosis and necroptosis

Zhao, Wen; Liu, Miao; Li, Jinfeng; Zhang, Hailin; Zhang, Hongkun; Han, Yongdian; Ba, Zhiwei; Zhang, Manli; Li, Dongdong; Liu, Chuanmiao

doi:10.1016/j.heliyon.2023.e15075

Cited by 6 publications

(2 citation statements)

References 53 publications

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“…Mannaerts and colleagues also demonstrated that YAP aberrant activation is an early event during fibrosis development, as YAP target genes ANKRD11 and CTGF, which are key components of fibrotic processes, are activated earlier than established markers of HSCs activation [ 77 , 80 ]. In agreement, YAP inhibition attenuated liver fibrosis in CCl 4 -induced liver fibrosis mouse model [ 81 , 82 ].…”

Section: Hippo Pathway Dysregulation On the Way To Liver Carcinogenesismentioning

confidence: 63%

Role of Hippo pathway dysregulation from gastrointestinal premalignant lesions to cancer

Schiavoni,

Messina,

Scalera

et al. 2024

J Transl Med

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Background First identified in Drosophila melanogaster, the Hippo pathway is considered a major regulatory cascade controlling tissue homeostasis and organ development. Hippo signaling components include kinases whose activity regulates YAP and TAZ final effectors. In response to upstream stimuli, YAP and TAZ control transcriptional programs involved in cell proliferation, cytoskeletal reorganization and stemness. Main text While fine tuning of Hippo cascade components is essential for maintaining the balance between proliferative and non-proliferative signals, pathway signaling is frequently dysregulated in gastrointestinal cancers. Also, YAP/TAZ aberrant activation has been described in conditions characterized by chronic inflammation that precede cancer development, suggesting a role of Hippo effectors in triggering carcinogenesis. In this review, we summarize the architecture of the Hippo pathway and discuss the involvement of signaling cascade unbalances in premalignant lesions of the gastrointestinal tract, providing a focus on the underlying molecular mechanisms. Conclusions The biology of premalignant Hippo signaling dysregulation needs further investigation in order to elucidate the evolutionary trajectories triggering cancer inititation and develop effective early therapeutic strategies targeting the Hippo/YAP pathway.

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Section: Hippo Pathway Dysregulation On the Way To Liver Carcinogenesismentioning

confidence: 63%

Role of Hippo pathway dysregulation from gastrointestinal premalignant lesions to cancer

Schiavoni,

Messina,

Scalera

et al. 2024

J Transl Med

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“… 106 The co-induction of liver fibrosis, ferroptosis, and necroptosis through Yes-associated protein (YAP) overexpression, a transcription factor in the Hippo pathway associated with liver fibrosis, can be alleviated by exosomes derived from human umbilical cord mesenchymal stem cells (huMSC-ex). 111 These exosomes have the ability to secrete BECN1, an autophagy regulator, through mediating ferritinophagy, which reduces system Xc-/GPX4. The decrease in system Xc-/GPX4 can significantly increase ferroptosis.…”

Section: The Crosstalk Between Different Types Of Pcdmentioning

confidence: 99%

Programmed Cell Death in Liver Fibrosis

Gao,

Tang,

Mao

2023

JIR

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Programmed cell death (PCD) is a comprehensive term that encompasses various forms of cell death, such as apoptosis, necroptosis, pyroptosis, ferroptosis, and autophagy, which play a crucial role in the pathogenesis of liver fibrosis. PCD facilitates the elimination of aberrant cells, particularly activated hepatic stellate cells (HSCs), which are the primary producers of extracellular matrix (ECM). The removal of HSCs may impede ECM synthesis, thereby mitigating liver fibrosis. As such, PCD has emerged as a promising therapeutic target for the development of novel drugs to treat liver fibrosis. Numerous studies have been conducted to investigate the underlying mechanisms of PCD in the elimination of activated HSCs and other aberrant liver cells in fibrotic liver tissue, including hepatocytes, hepatic sinusoid endothelial cells (LSECs), and Kupffer cells (KCs). The induction of PCD, the interplay between different forms of PCD, and the potential harm or benefit of PCD in liver fibrosis are topics of ongoing research. Evidences suggest that PCD is a complex process with dual effects on liver fibrosis. The purpose of this review is to summarize the most recent advances in PCD and liver fibrosis research.

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Yes-associated protein inhibition ameliorates carbon tetrachloride-induced acute liver injury in mice by reducing VDR

Wang,

Pan,

Gong

et al. 2024

Chemico-Biological Interactions

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Yes-associated protein inhibition ameliorates liver fibrosis and acute and chronic liver failure by decreasing ferroptosis and necroptosis

Cited by 6 publications

References 53 publications

Role of Hippo pathway dysregulation from gastrointestinal premalignant lesions to cancer

Role of Hippo pathway dysregulation from gastrointestinal premalignant lesions to cancer

Programmed Cell Death in Liver Fibrosis

Yes-associated protein inhibition ameliorates carbon tetrachloride-induced acute liver injury in mice by reducing VDR

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