Interaction of non‑parenchymal hepatocytes in the process of hepatic fibrosis (Review)

Cheng, Qi-Ni; Yang, Xue; Wu, Jiangfeng; Ai, Wen-Bing; Ni, Yi-Ran

doi:10.3892/mmr.2021.12003

Cited by 14 publications

(9 citation statements)

References 120 publications

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“…The liver's parenchymal and nonparenchymal cells both contribute to LC and liver fibrosis. [26] Flavonoids are divided into several families due to structural differences in the C-ring core: flavones, flavonols, flavanones, coumestans, dihydroflavonols, catechins, chalcones, isoflavones, and anthocyanidins as depicted in Figure 3-11. [27] Flavonoids have been shown to benefit alcohol, non-alcohol, viral infection, fatty acids, and other factors that contribute to LC by decreasing lipid metabolism, oxidative stress, inflammation, insulin resistance, apoptosis, cellular proliferation, tumor, and cytokines.…”

Section: Flavonoids Protect Liver Cirrhosis By Cellular and Molecular...mentioning

confidence: 99%

“…Hepatic sinusoids are bordered by nonparenchymal cells such as liver sinusoidal endothelial cells (LSECs), Kupffer cells (KCs), and HSCs. The liver's parenchymal and nonparenchymal cells both contribute to LC and liver fibrosis [26] . Flavonoids are divided into several families due to structural differences in the C‐ring core: flavones, flavonols, flavanones, coumestans, dihydroflavonols, catechins, chalcones, isoflavones, and anthocyanidins as depicted in Figure 345678910 – 11 [27] .…”

Section: Flavonoids Protect Liver Cirrhosis By Cellular and Molecular...mentioning

confidence: 99%

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The Preventive and Therapeutic Potential of the Flavonoids in Liver Cirrhosis: Current and Future Perspectives

Sahu

Goswami

Sastry

et al. 2023

Chemistry & Biodiversity

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Non‐alcoholic fatty liver disease (NAFLD) may vary from moderately mild non‐alcohol fatty liver (NAFL) towards the malignant variant known as non‐alcoholic steatohepatitis (NASH), which is marked by fatty liver inflammation and may progress to liver cirrhosis (LC), liver cancer, fibrosis, or liver failure. Flavonoids can protect the liver from toxins through their anti‐inflammatory, antioxidant, anti‐cancer, and antifibrogenic pharmacological activities. Furthermore, flavonoids protect against LC by regulation of hepatic stellate cells (HSCs) trans‐differentiation, inhibiting growth factors like TGF‐β and platelets‐derived growth factor (PDGF), vascular epithelial growth factor (VEGF), viral infections like hepatitis‐B, C and D viruses (HBV, HCV & HDV), autoimmune‐induced, alcohol‐induced, metabolic disorder‐induced, causing by apoptosis, and regulating MAPK pathways. These flavonoids may be explored in the future as a therapeutic solution for hepatic diseases.

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Section: Flavonoids Protect Liver Cirrhosis By Cellular and Molecular...mentioning

confidence: 99%

Section: Flavonoids Protect Liver Cirrhosis By Cellular and Molecular...mentioning

confidence: 99%

The Preventive and Therapeutic Potential of the Flavonoids in Liver Cirrhosis: Current and Future Perspectives

Sahu

Goswami

Sastry

et al. 2023

Chemistry & Biodiversity

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“…Even more likely, the overproduction of cytokines and iNOS by hepatic Kupffer cells (KCs) and monocytes and lymphocytes stimulates a proinflammatory environment [ 179 ]. ROS produced by KCs stimulate HSCs by increasing the proliferation and production of extracellular matrices, which contributes to fibrosis and cirrhosis ( Figure 3 ) [ 180 ]. Oxidative stress, in combination with inflammation, generates localized or zonal necrosis, hepatocyte death, and architectural disturbance [ 181 ].…”

Section: Possible Interaction Mechanisms Among Coagulation Dyshomeost...mentioning

confidence: 99%

Coagulation Dysfunctions in Non-Alcoholic Fatty Liver Disease—Oxidative Stress and Inflammation Relevance

Robea,

Balmus,

Girleanu

et al. 2023

Medicina

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Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases. Its incidence is progressively rising and it is possibly becoming a worldwide epidemic. NAFLD encompasses a spectrum of diseases accounting for the chronic accumulation of fat within the hepatocytes due to various causes, excluding excessive alcohol consumption. In this study, we aimed to focus on finding evidence regarding the implications of oxidative stress and inflammatory processes that form the multifaceted pathophysiological tableau in relation to thrombotic events that co-occur in NAFLD and associated chronic liver diseases. Recent evidence on the pathophysiology of NAFLD suggests that a complex pattern of multidirectional components, such as prooxidative, proinflammatory, and prothrombotic components, better explains the multiple factors that promote the mechanisms underlying the fatty acid excess and subsequent processes. As there is extensive evidence on the multi-component nature of NAFLD pathophysiology, further studies could address the complex interactions that underlie the development and progression of the disease. Therefore, this study aimed to describe possible pathophysiological mechanisms connecting the molecular impairments with the various clinical manifestations, focusing especially on the interactions among oxidative stress, inflammation, and coagulation dysfunctions. Thus, we described the possible bidirectional modulation among coagulation homeostasis, oxidative stress, and inflammation that occurs in the various stages of NAFLD.

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“…The normal subendothelial ECM is an elaborate cross-linked network of multiple proteins (e.g., such as collagens, elastins, fibronectins, laminins) and composition is fundamental to maintain all the different function of the liver cells and tissue homeostasis [ 55 ]. A plethora of signals can cause matrix and cellular alterations and, therefore, determine the initiation and progression of liver disorders, such as the following: the release of PAMPs (e.g., LPS, lipoteichoic acid (LTA), and β-glucan; the release of DAMPs by damaged/dead hepatocytes (e.g., high mobility group box 1 (HMGB1), mitochondrial DNA (mtDNA), and ATP); the release of reactive oxygen species (ROS) by damaged/dead hepatocytes; an hypoxic environment (e.g., due to the enhanced expression of hypoxia-inducible factor (HIF)-1α) [ 56 ]. All the signals lead to the activation of HSCs and KFs.…”

Section: Macrophages and Liver Fibrosismentioning

confidence: 99%

The Role of Macrophages in Liver Fibrosis: New Therapeutic Opportunities

Binatti

Gerussi

Barisani

et al. 2022

IJMS

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Chronic inflammation is the hallmark of fibrotic disorders and is characterized by the activation of immune cells in the damaged tissues. Macrophages have emerged as central players in the fibrotic process since they initiate, sustain and amplify the inflammatory reaction. As regards the liver, distinct populations of phagocytic cells, like Kupffer cells and monocyte-derived macrophages, are indisputably key cells implicated in the pathogenesis of several chronic liver diseases. In this review, we summarize the current knowledge on the origin, role and functions of macrophages in fibrotic conditions, with a specific focus on liver fibrosis; then, we discuss some innovative therapeutic strategies targeting macrophages in fibrotic liver diseases.

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Interaction of non‑parenchymal hepatocytes in the process of hepatic fibrosis (Review)

Cited by 14 publications

References 120 publications

The Preventive and Therapeutic Potential of the Flavonoids in Liver Cirrhosis: Current and Future Perspectives

The Preventive and Therapeutic Potential of the Flavonoids in Liver Cirrhosis: Current and Future Perspectives

Coagulation Dysfunctions in Non-Alcoholic Fatty Liver Disease—Oxidative Stress and Inflammation Relevance

The Role of Macrophages in Liver Fibrosis: New Therapeutic Opportunities

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