Indoleamine 2, 3-dioxygenase 1enhanceshepatocytes ferroptosis in acute immune hepatitis associated with excess nitrative stress

Zeng, Ting; Deng, Guanghui; Zhong, Wu; Gao, Zhuowei; Ma, Shuoyi; Mo, Chan; Li, Yunjia; Huang, Sha; Zhou, Chuying; Lai, Yuqi; Xie, Shuwen; Xie, Zeping; Chen, Yuyao; He, Songqing; Lv, Zhen; Gao, Lei

doi:10.1016/j.freeradbiomed.2020.01.009

Cited by 52 publications

(36 citation statements)

References 64 publications

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“…et al, 2018;Hirata et al, 2019), although oxytosis has long been considered to be the main mode leading to neuronal cell damage caused by glutamate toxicity (Tan et al, 2001). Inflammation mediated by ferroptotic cell death can promote pancreatitis (Liu et al, 2020d), liver fibrosis (Tsurusaki et al, 2019;Zeng et al, 2020), chronic obstructive pulmonary disease (COPD) (Park et al, 2019;Wang and Tang, 2019;Yoshida et al, 2019), inflammatory bowel disease (Mayr et al, 2020), and preeclampsia (Zhang et al, 2020). In addition, inhibiting ferroptosis can prevent I/R damage to various tissues, especially liver, kidney, brain, and heart (Linkermann et al, 2014;Skouta et al, 2014;Martin-Sanchez et al, 2017;Muller et al, 2017;Fang et al, 2019).…”

Section: Ferroptosis In Diseasementioning

confidence: 99%

Oxidative Damage and Antioxidant Defense in Ferroptosis

Kuang

Liu

Tang

et al. 2020

Front. Cell Dev. Biol.

354

197

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Many new types of regulated cell death have been recently implicated in human health and disease. These regulated cell deaths have different morphological, genetic, biochemical, and functional hallmarks. Ferroptosis was originally described as a carcinogenic RAS-dependent non-apoptotic cell death, and is now defined as a type of regulated necrosis characterized by iron accumulation, lipid peroxidation, and the release of damage-associated molecular patterns (DAMPs). Multiple oxidative and antioxidant systems, acting together autophagy machinery, shape the process of lipid peroxidation during ferroptosis. In particular, the production of reactive oxygen species (ROS) that depends on the activity of nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs) and the mitochondrial respiratory chain promotes lipid peroxidation by lipoxygenase (ALOX) or cytochrome P450 reductase (POR). In contrast, the glutathione (GSH), coenzyme Q10 (CoQ10), and tetrahydrobiopterin (BH 4) system limits oxidative damage during ferroptosis. These antioxidant processes are further transcriptionally regulated by nuclear factor, erythroid 2-like 2 (NFE2L2/NRF2), whereas membrane repair during ferroptotic damage requires the activation of endosomal sorting complexes required for transport (ESCRT)-III. A further understanding of the process and function of ferroptosis may provide precise treatment strategies for disease.

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Section: Ferroptosis In Diseasementioning

confidence: 99%

Oxidative Damage and Antioxidant Defense in Ferroptosis

Kuang

Liu

Tang

et al. 2020

Front. Cell Dev. Biol.

354

197

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“…Previously, we observed that serum IDO1 level was decreased in patients with HBV-induced cirrhosis as compared to healthy volunteers, whereas serum IDO1 was dramatically increased in fibrotic mice induced by CCL4 14 . In a recent study by our group, we reported that IDO1 acted as an important factor that triggered RNS stress, contributed to ferritin degradation and further caused ferroptosis in ConA-induced liver injury 15 . However, it was reported that IDO might have a protective effect against hepatic fibrosis in HFD-induced liver injury model 27 .…”

Section: Discussionmentioning

confidence: 92%

“…Given these points, it is not difficult to understand why different animal models have different experimental results. Additionally, published literatures showing that the inhibition of IDO1 may be used to treat chronic HCV patients in vivo and the inhibition of IDO1 could alleviate murine liver damage with the reduction of inducible nitric oxide synthase and 3-nitrotyrosine expression 15,32 . It has been reported that IDO1 functions as a pro-fibrogenesis factor in CCL4-induced liver fibrosis 33,34 .…”

Section: Discussionmentioning

confidence: 99%

“…A relevant study figured out that knock out of IDO1 reduced Th17 cells and further protected mice from CCL4-induced liver fibrosis 14 . IDO1 was dramatically upregulated during concanavalin A-induced acute immune hepatitis and inhibited of IDO1 could alleviate murine hepatic damage 15 . Several lines of evidence suggest that IDO1 is involved in regulating several kinds of immune cells.…”

Section: Introductionmentioning

confidence: 99%

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Indoleamine 2,3-dioxygenase 1 limits hepatic inflammatory cells recruitment and promotes bile duct ligation-induced liver fibrosis

Xie

Liu

et al. 2021

Cell Death Dis

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Liver fibrosis is a course of chronic liver dysfunction, can develop into cirrhosis and hepatocellular carcinoma. Inflammatory insult owing to pathogenic factors plays a crucial role in the pathogenesis of liver fibrosis. Indoleamine 2,3-dioxygenase 1 (IDO1) can affect the infiltration of immune cells in many pathology processes of diseases, but its role in liver fibrosis has not been elucidated completely. Here, the markedly elevated protein IDO1 in livers was identified, and dendritic cells (DCs) immune-phenotypes were significantly altered after BDL challenge. A distinct hepatic population of CD11c+DCs was decreased and presented an immature immune-phenotype, reflected by lower expression levels of co-stimulatory molecules (CD40, MHCII). Frequencies of CD11c+CD80+, CD11c+CD86+, CD11c+MHCII+, and CD11c+CD40+ cells in splenic leukocytes were reduced significantly. Notably, IDO1 overexpression inhibited hepatic, splenic CD11c+DCs maturation, mature DCs-mediated T-cell proliferation and worsened liver fibrosis, whereas above pathological phenomena were reversed in IDO1−/− mice. Our data demonstrate that IDO1 affects the process of immune cells recruitment via inhibiting DCs maturation and subsequent T cells proliferation, resulting in the promotion of hepatic fibrosis. Thus, amelioration of immune responses in hepatic and splenic microenvironment by targeting IDO1 might be essential for the therapeutic effects on liver fibrosis.

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“…Indoleamine 2,3-dioxygenase 1 (IDO1) is an intracellular heme enzyme, which serves as an important immune regulator and is related to the production of Fe 2+ 81,82 . Intervention of IDO1 and the administration of ferroptosis inhibitor mitigated ferroptotic cell death and nitrative stress in the ConA-challenged mice 83 . The underpinning mechanism of IDO1-dependent ferroptosis comprises its role of system x c − modulator as well as versatile inflammatory state modifier.…”

Section: Immune-mediated Hepatitismentioning

confidence: 94%

The emerging role of ferroptosis in non-cancer liver diseases: hype or increasing hope?

et al. 2020

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Ferroptosis is an iron- and lipotoxicity-dependent form of regulated cell death (RCD). It is morphologically and biochemically distinct from characteristics of other cell death. This modality has been intensively investigated in recent years due to its involvement in a wide array of pathologies, including cancer, neurodegenerative diseases, and acute kidney injury. Dysregulation of ferroptosis has also been linked to various liver diseases and its modification may provide a hopeful and attractive therapeutic concept. Indeed, targeting ferroptosis may prevent the pathophysiological progression of several liver diseases, such as hemochromatosis, nonalcoholic steatohepatitis, and ethanol-induced liver injury. On the contrary, enhancing ferroptosis may promote sorafenib-induced ferroptosis and pave the way for combination therapy in hepatocellular carcinoma. Glutathione peroxidase 4 (GPx4) and system xc− have been identified as key players to mediate ferroptosis pathway. More recently diverse signaling pathways have also been observed. The connection between ferroptosis and other forms of RCD is intricate and compelling, where discoveries in this field advance our understanding of cell survival and fate. In this review, we summarize the central molecular machinery of ferroptosis, describe the role of ferroptosis in non-cancer hepatic disease conditions and discuss the potential to manipulate ferroptosis as a therapeutic strategy.

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Indoleamine 2, 3-dioxygenase 1enhanceshepatocytes ferroptosis in acute immune hepatitis associated with excess nitrative stress

Cited by 52 publications

References 64 publications

Oxidative Damage and Antioxidant Defense in Ferroptosis

Oxidative Damage and Antioxidant Defense in Ferroptosis

Indoleamine 2,3-dioxygenase 1 limits hepatic inflammatory cells recruitment and promotes bile duct ligation-induced liver fibrosis

The emerging role of ferroptosis in non-cancer liver diseases: hype or increasing hope?

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