Hypoxia, Hypoxia-Inducible Factors and Liver Fibrosis

Foglia, Beatrice; Novo, Erica; Protopapa, Francesca; Maggiora, Marina; Bocca, Claudia; Cannito, Stefania; Parola, Maurizio

doi:10.3390/cells10071764

Cited by 37 publications

(29 citation statements)

References 153 publications

(399 reference statements)

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“…Lastly, the arterial blood gases were evaluated, both due to the lung and liver affinity of the SARS-CoV-2 [28], and due to the mild hypoxemia encountered by approximately one-third of patients with chronic liver disease [29]. This anomaly can be explained by the findings that arterial venous anastomoses and communications between the portal and arterial circulations, as well as between the bronchial and pulmonary veins, are more likely to be functional in patients with cirrhosis.…”

Section: Discussionmentioning

confidence: 99%

Laboratory Profile of COVID-19 Patients with Hepatitis C-Related Liver Cirrhosis

Cerbu

Grigoraş

Bratosin

et al. 2022

JCM

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Patients with cirrhosis are known to have multiple comorbidities and impaired organ system functioning due to alterations caused by chronic liver failure. In the past two years, since the COVID-19 pandemic started, several studies have described the affinity of SARS-CoV-2 with the liver and biliary cells. Considering hepatitis C as a significant independent factor for cirrhosis in Romania, this research was built on the premises that this certain group of patients is susceptible to alterations of their serum parameters that are yet to be described, which might be useful in the management of COVID-19 in these individuals. A retrospective cohort study was developed at a tertiary hospital for infectious disease in Romania, which included a total of 242 patients with hepatitis C cirrhosis across two years, out of which 46 patients were infected with SARS-CoV-2. Stratification by patient weight and COVID-19 status identified several important laboratory serum tests as predictors for acute-on-chronic liver failure and risk for intensive care unit admission. Thus, white blood cell count, lymphocyte count, ferritin, hypoglycemia, prothrombin time, and HCV viral load were independent risk factors for ACLF in patients with COVID-19. High PT, creatinine, BUN, and HCV viral load were the strongest predictors for ICU admission. Inflammatory markers and parameters of gas exchange were also observed as risk factors for ACLF and ICU admission, including procalcitonin, CRP, IL-6, and D-dimers. Our study questions and confirms the health impact of COVID-19 on patients with cirrhosis and whether their laboratory profile significantly changes due to SARS-CoV-2 infection.

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Section: Discussionmentioning

confidence: 99%

Laboratory Profile of COVID-19 Patients with Hepatitis C-Related Liver Cirrhosis

Cerbu

Grigoraş

Bratosin

et al. 2022

JCM

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“…The development of NAFLD is closely related to hypoxia [ 270 ]. Experimental data showed that a high-fat diet resulted in severe hypoxia and triglyceride accumulation in the liver of mice [ 271 ].…”

Section: Lipid Metabolism Disorders In the Development And Progression Of Copdmentioning

confidence: 99%

Lipid Metabolism Disorders in the Comorbid Course of Nonalcoholic Fatty Liver Disease and Chronic Obstructive Pulmonary Disease

Kotlyarov

Bulgakov

2021

Cells

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Non-alcoholic fatty liver disease (NAFLD) is currently among the most common liver diseases. Unfavorable data on the epidemiology of metabolic syndrome and obesity have increased the attention of clinicians and researchers to the problem of NAFLD. The research results allow us to emphasize the systemicity and multifactoriality of the pathogenesis of liver parenchyma lesion. At the same time, many aspects of its classification, etiology, and pathogenesis remain controversial. Local and systemic metabolic disorders are also a part of the pathogenesis of chronic obstructive pulmonary disease and can influence its course. The present article analyzes the metabolic pathways mediating the links of impaired lipid metabolism in NAFLD and chronic obstructive pulmonary disease (COPD). Free fatty acids, cholesterol, and ceramides are involved in key metabolic and inflammatory pathways underlying the pathogenesis of both diseases. Moreover, inflammation and lipid metabolism demonstrate close links in the comorbid course of NAFLD and COPD.

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“…The altered ECM remodeling observed is due to up-regulation of the expression of TIMPs and MMPs accompanied by the non-efficient removal of fibrillar collagen [ 1 , 5 , 6 , 7 , 8 , 9 ]. Hypoxia, HIFs, and related mediators are considered major determinants for fibrogenic progression and likely also for the development of hepatocellular carcinoma [ 47 ]. Autophagy and endoplasmic reticulum stress are mechanisms involved in the activation of HSCs into HSC/MFs, with the inositol-requiring enzyme 1α (IRE1α) and PKR-like endoplasmic reticulum kinase (PERK) pathways playing a pro-fibrogenic role [ 48 , 49 ].…”

Section: Mfs Involvement In the Scenario Of Liver Fibrogenesismentioning

confidence: 99%

“…Hypoxia, HIFs, and related mediators are considered major determinants for fibrogenic progression and likely also for the development of hepatocellular carcinoma [ 47 ].…”

Section: Mfs Involvement In the Scenario Of Liver Fibrogenesismentioning

confidence: 99%

“…Hypoxia, HIFs, and related mediators are considered major determinants for fibrogenic progression and likely also for the development of hepatocellular carcinoma [47]. All mechanisms described represent the basic knowledge for developing novel strategies and approaches to targeted therapies designed to affect CLD progression and have actually been tested in clinical trials.…”

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confidence: 99%

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Hepatic Myofibroblasts: A Heterogeneous and Redox-Modulated Cell Population in Liver Fibrogenesis

et al. 2022

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During chronic liver disease (CLD) progression, hepatic myofibroblasts (MFs) represent a unique cellular phenotype that plays a critical role in driving liver fibrogenesis and then fibrosis. Although they could originate from different cell types, MFs exhibit a rather common pattern of pro-fibrogenic phenotypic responses, which are mostly elicited or sustained both by oxidative stress and reactive oxygen species (ROS) and several mediators (including growth factors, cytokines, chemokines, and others) that often operate through the up-regulation of the intracellular generation of ROS. In the present review, we will offer an overview of the role of MFs in the fibrogenic progression of CLD from different etiologies by focusing our attention on the direct or indirect role of ROS and, more generally, oxidative stress in regulating MF-related phenotypic responses. Moreover, this review has the purpose of illustrating the real complexity of the ROS modulation during CLD progression. The reader will have to keep in mind that a number of issues are able to affect the behavior of the cells involved: a) the different concentrations of reactive species, b) the intrinsic state of the target cells, as well as c) the presence of different growth factors, cytokines, and other mediators in the extracellular microenvironment or of other cellular sources of ROS.

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Hypoxia, Hypoxia-Inducible Factors and Liver Fibrosis

Cited by 37 publications

References 153 publications

Laboratory Profile of COVID-19 Patients with Hepatitis C-Related Liver Cirrhosis

Laboratory Profile of COVID-19 Patients with Hepatitis C-Related Liver Cirrhosis

Lipid Metabolism Disorders in the Comorbid Course of Nonalcoholic Fatty Liver Disease and Chronic Obstructive Pulmonary Disease

Hepatic Myofibroblasts: A Heterogeneous and Redox-Modulated Cell Population in Liver Fibrogenesis

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