scholarly journals The Potential Application of Magnetic Nanoparticles for Liver Fibrosis Theranostics

2021 ◽  
Vol 9 ◽  
Author(s):  
Aziz Eftekhari ◽  
Allahveirdy Arjmand ◽  
Ayyub Asheghvatan ◽  
Helena Švajdlenková ◽  
Ondrej Šauša ◽  
...  
Keyword(s):  
Magnetic Nanoparticles ◽  
Liver Fibrosis ◽  
Hepatic Fibrosis ◽  
Liver Diseases ◽  
Molecular Mechanisms ◽  
Tissue Penetration ◽  
Specific Therapy ◽  
Chronic Liver Damage ◽  
Superparamagnetic Properties ◽  
New Strategies

Liver fibrosis is a major cause of morbidity and mortality worldwide due to chronic liver damage and leading to cirrhosis, liver cancer, and liver failure. To date, there is no effective and specific therapy for patients with hepatic fibrosis. As a result of their various advantages such as biocompatibility, imaging contrast ability, improved tissue penetration, and superparamagnetic properties, magnetic nanoparticles have a great potential for diagnosis and therapy in various liver diseases including fibrosis. In this review, we focus on the molecular mechanisms and important factors for hepatic fibrosis and on potential magnetic nanoparticles-based therapeutics. New strategies for the diagnosis of liver fibrosis are also discussed, with a summary of the challenges and perspectives in the translational application of magnetic nanoparticles from bench to bedside.

scholarly journals Systematic profiling of the effective ingredients and mechanism of Scabiosa comosa and S. tschilliensis against hepatic fibrosis combined with network pharmacology

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Qianwen Chen ◽  
Yuanyuan Wang ◽  
Feixiang Ma ◽  
Mengdi Han ◽  
Zhen Wang ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Hepatic Fibrosis ◽  
Liver Diseases ◽  
Molecular Mechanisms ◽  
Enrichment Analysis ◽  
Network Pharmacology ◽  
Chain Reaction ◽  
The Common ◽  
Polymerase Chain ◽  
Omim Database

AbstractScabiosa comosa and S. tschilliensis (SCST) are traditionally used for liver diseases in Mongolian medicine. However, their active ingredients and molecular mechanisms are unknown. The present study employed network pharmacology and experimental verification approaches to decipher the common pharmacological mechanisms of SCST on liver fibrosis, which is the key step in liver diseases. We predicted the targets of all available SCST ingredients with the SWISS and SuperPred servers and clustered the targets related to liver fibrosis from DrugBank, the OMIM database and the literature. We further evaluated the links between the herbal ingredients and pharmacological actions to explore the potential mechanism of action of SCST. We found that the PPARG signalling pathway could be regulated by SCST for liver fibrosis through enrichment analysis. The key targets included 8 co-targets, including HSP90AA1, PPARG, HSP90AB1, STAT1, etc., which play pivotal roles in the pathogenesis of liver fibrosis. Additionally, the top 15 key compounds included flavonoids and phenylpropanoids. Central to the pathogenesis of liver fibrosis is trans-differentiation or activation of hepatic stellate cells (HSCs). Therefore, LX2 cells, an immortalized human HSC line, were studied. Here, a total 37 components were isolated and identified from the inflorescences of SCST, including the new compound tschilliensisin, and the first separated components, β-sitosterol and luteolin, and these compounds were assessed against anti-hepatic fibrosis. An MTT assay and quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting analyses demonstrated that the flavonoids of SCST revealed anti-hepatic fibrosis effects via anti-proliferation and increases in the Stat1, Pparg, Hsp90aa1 genes and STAT1 and PPARG proteins in LX-2 cells. In conclusion, these results indicate that SCST has multi-targeted and multi-component synergistic anti-hepatic fibrosis effects.

scholarly journals The roles and mechanisms of hypoxia in liver fibrosis

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Jingyao Cai ◽  
Min Hu ◽  
Zhiyang Chen ◽  
Zeng Ling
Keyword(s):  
Quality Of Life ◽  
Liver Fibrosis ◽  
Theoretical Basis ◽  
Liver Diseases ◽  
Molecular Mechanisms ◽  
Clinical Intervention ◽  
Chronic Liver Injury ◽  
Key Factor

AbstractLiver fibrosis occurs in response to any etiology of chronic liver injury. Lack of appropriate clinical intervention will lead to liver cirrhosis or hepatocellular carcinoma (HCC), seriously affecting the quality of life of patients, but the current clinical treatments of liver fibrosis have not been developed yet. Recent studies have shown that hypoxia is a key factor promoting the progression of liver fibrosis. Hypoxia can cause liver fibrosis. Liver fibrosis can, in turn, profoundly further deepen the degree of hypoxia. Therefore, exploring the role of hypoxia in liver fibrosis will help to further understand the process of liver fibrosis, and provide the theoretical basis for its diagnosis and treatment, which is of great significance to avoid further deterioration of liver diseases and protect the life and health of patients. This review highlights the recent advances in cellular and molecular mechanisms of hypoxia in developments of liver fibrosis.

scholarly journals Natural Sulfur-Containing Compounds: An Alternative Therapeutic Strategy against Liver Fibrosis

Cells ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 1356 ◽  
Author(s):  
Milito ◽  
Brancaccio ◽  
D’Argenio ◽  
Castellano
Keyword(s):  
Extracellular Matrix ◽  
Growth Factor ◽  
Liver Fibrosis ◽  
Hepatic Fibrosis ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Extracellular Matrix Proteins ◽  
Matrix Proteins ◽  
Sulfur Containing ◽  
Sulfur Containing Compounds

Liver fibrosis is a pathophysiologic process involving the accumulation of extracellular matrix proteins as collagen deposition. Advanced liver fibrosis can evolve in cirrhosis, portal hypertension and often requires liver transplantation. At the cellular level, hepatic fibrosis involves the activation of hepatic stellate cells and their transdifferentiation into myofibroblasts. Numerous pro-fibrogenic mediators including the transforming growth factor-β1, the platelet-derived growth factor, endothelin-1, toll-like receptor 4, and reactive oxygen species are key players in this process. Knowledge of the cellular and molecular mechanisms underlying hepatic fibrosis development need to be extended to find novel therapeutic strategies. Antifibrotic therapies aim to inhibit the accumulation of fibrogenic cells and/or prevent the deposition of extracellular matrix proteins. Natural products from terrestrial and marine sources, including sulfur-containing compounds, exhibit promising activities for the treatment of fibrotic pathology. Although many therapeutic interventions are effective in experimental models of liver fibrosis, their efficacy and safety in humans are largely unknown. This review aims to provide a reference collection on experimentally tested natural anti-fibrotic compounds, with particular attention on sulfur-containing molecules. Their chemical structure, sources, mode of action, molecular targets, and pharmacological activity in the treatment of liver disease will be discussed.

scholarly journals LncRNAs Act as a Link between Chronic Liver Disease and Hepatocellular Carcinoma

2020 ◽  
Vol 21 (8) ◽  
pp. 2883
Author(s):  
Young-Ah Kim ◽  
Kwan-Kyu Park ◽  
Sun-Jae Lee
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Disease ◽  
Chronic Liver Disease ◽  
Hepatic Fibrosis ◽  
Liver Diseases ◽  
Molecular Mechanisms ◽  
Chronic Liver ◽  
Chronic Liver Diseases ◽  
Nonalcoholic Fatty Liver ◽  
Underlying Mechanisms

Long non-coding RNAs (lncRNAs) are emerging as important contributors to the biological processes underlying the pathophysiology of various human diseases, including hepatocellular carcinoma (HCC). However, the involvement of these molecules in chronic liver diseases, such as nonalcoholic fatty liver disease (NAFLD) and viral hepatitis, has only recently been considered in scientific research. While extensive studies on the pathogenesis of the development of HCC from hepatic fibrosis have been conducted, their regulatory molecular mechanisms are still only partially understood. The underlying mechanisms related to lncRNAs leading to HCC from chronic liver diseases and cirrhosis have not yet been entirely elucidated. Therefore, elucidating the functional roles of lncRNAs in chronic liver disease and HCC can contribute to a better understanding of the molecular mechanisms, and may help in developing novel diagnostic biomarkers and therapeutic targets for HCC, as well as in preventing the progression of chronic liver disease to HCC. Here, we comprehensively review and briefly summarize some lncRNAs that participate in both hepatic fibrosis and HCC.

scholarly journals The role of miR-29a in the regulation, function, and signaling of liver fibrosis

2018 ◽  
Author(s):  
Ying-Hsien Huang ◽  
Ya-Ling Yang ◽  
Feng-Sheng Wang
Keyword(s):  
Liver Fibrosis ◽  
Molecular Mechanisms ◽  
Stellate Cells ◽  
Experimental Therapy ◽  
Complete Understanding ◽  
Chronic Liver Damage ◽  
Clinical Challenge ◽  
Non Coding Rna ◽  
Regulation Function

Both fibrosis and cirrhosis of the liver are the end results of most kinds of chronic liver damage and present a common but difficult clinical challenge throughout the world. The inhibition of the fibrogenic, proliferative, and migratory effects of hepatic stellate cells (HSCs) has become an experimental therapy for preventing and even reversing hepatic fibrosis. Furthermore, a complete understanding of the function of non-coding RNA-mediated epigenetic mechanisms in HSC activation may improve our perception of liver fibrosis pathogenesis. This review focuses on an evolving view of molecular mechanisms in which HSC activation by miR-29a signaling may moderate their profibrogenic phenotype, thus supporting the use of miR-29a agonists as a potential therapy for treating liver fibrosis in the future.

Molecular mechanisms of hepatic fibrosis in chronic liver diseases

2020 ◽  
Vol 32 (3) ◽  
Author(s):  
Chiara Rosso ◽  
Gian Paolo Caviglia ◽  
Ramy Younes ◽  
Davide G. Ribaldone ◽  
Sharmila Fagoonee ◽  
...  
Keyword(s):  
Hepatic Fibrosis ◽  
Liver Diseases ◽  
Molecular Mechanisms ◽  
Chronic Liver ◽  
Chronic Liver Diseases

scholarly journals Hepatic necroinflammation and severe liver fibrosis in patients with chronic hepatitis B with undetectable HBV DNA and persistently normal alanine aminotransferase

2015 ◽  
Vol 40 (3) ◽  
pp. 92-96 ◽  
Author(s):  
MM Alam ◽  
MA Mahtab ◽  
SMF Akbar ◽  
M Kamal ◽  
S Rahman
Keyword(s):  
Chronic Hepatitis ◽  
Liver Fibrosis ◽  
Hepatitis B ◽  
Chronic Hepatitis B ◽  
Hepatic Fibrosis ◽  
Alanine Aminotransferase ◽  
Liver Diseases ◽  
Hbv Dna ◽  
Treatment Recommendation ◽  
Normal Alt

Both consensus and controversy remains regarding surrogacy of hepatitis B virus (HBV) deoxyribonucleic acid (DNA) and alanine aminotransferase (ALT), however, these markers are used to ascertain the extent of liver damages and to guide therapeutic options in patients with chronic hepatitis B. However, little is known about liver histology of patients with chronic hepatitis B with undetectable HBV DNA and persistently normal ALT. Thirty-five incidentally-detected patients with chronic HBV infection (assessed by expression of hepatitis B surface antigen for more than 6 months) with undetectable HBV DNA and normal serum ALT were enrolled in this study. Liver biopsy specimens were taken from all patients and the extent of hepatic necroinflammation and liver fibrosis were evaluated. Moderate degree of hepatic necroinflammation was detected in 2 of 35 patients and severe hepatic fibrosis was seen in 6 of 35 patients. Two patients with undetectable HBV DNA and sustained normal ALT had moderate hepatic necroinflammation and severe hepatic fibrosis. In spite of undetectable HBV DNA for prolonged period and persistently normal ALT, some patients with chronic hepatitis B express evidences of progressive liver diseases. Large scale studies in different races and geographical regions should be accomplished to develop insights about management of these patients. Studies about extent of liver diseases in these patients should be accomplished in Treatment recommendation and management strategies should be developed for these patients.Bangladesh Med Res Counc Bull 2014; 40 (3): 92-96

HEPATIC FIBROSIS: Molecular Mechanisms and Drug Targets

2005 ◽  
Vol 45 (1) ◽  
pp. 605-628 ◽  
Author(s):  
Sophie Lotersztajn ◽  
Boris Julien ◽  
Fatima Teixeira-Clerc ◽  
Pascale Grenard ◽  
Ariane Mallat
Keyword(s):  
Liver Fibrosis ◽  
Hepatic Fibrosis ◽  
Drug Targets ◽  
Molecular Mechanisms ◽  
Current Treatment ◽  
Culture Studies ◽  
Common Response ◽  
The Common ◽  
Parenchymal Injury ◽  
Antifibrotic Drugs

Liver fibrosis is the common response to chronic liver injury, ultimately leading to cirrhosis and its complications, portal hypertension, liver failure, and hepatocellular carcinoma. Efficient and well-tolerated antifibrotic drugs are currently lacking, and current treatment of hepatic fibrosis is limited to withdrawal of the noxious agent. Efforts over the past decade have mainly focused on fibrogenic cells generating the scarring response, although promising data on inhibition of parenchymal injury and/or reduction of liver inflammation have also been obtained. A large number of approaches have been validated in culture studies and in animal models, and several clinical trials are underway or anticipated for a growing number of molecules. This review highlights recent advances in the molecular mechanisms of liver fibrosis and discusses mechanistically based strategies that have recently emerged.

scholarly journals The Predictive Value of Mean Platelet Volume for Liver Fibrosis in Children With Chronic Liver Diseases

2020 ◽  
Vol 5 (4) ◽  
pp. 131-135
Author(s):  
Seyed Mohsen Dehghani ◽  
Mohammad Reza Bordbar ◽  
Rezvan Salimi ◽  
Iraj Shahramian ◽  
Hadi Mirzae ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Predictive Value ◽  
Mean Platelet Volume ◽  
Liver Diseases ◽  
Clinical Presentation ◽  
Chronic Liver ◽  
Chronic Liver Diseases ◽  
Platelet Volume ◽  
Chronic Liver Damage ◽  
Almost All

Introduction: Almost all causes of chronic liver damage can culminate in liver fibrosis and ultimately cirrhosis. Studies have suggested a relationship between mean platelet volume (MPV) and liver fibrosis; however, this needs confirmation by further studies. We here assessed the predictive value of MPV for liver fibrosis in children with chronic liver diseases. Methods: In this study, children <18 years old with chronic liver diseases referred to the Nemazee Hospital of Shiraz during 2013-2016 were studied. The patients underwent liver biopsy for assessing liver fibrosis. Statistical analyses were conducted in SPSS 23. Results: From 368 studied children, 52.2% were boys. The patients’ mean age was 4.5±3.9 years old. Most patients had grade 6 fibrosis (36.7%). Cryptogenic (42.7%) was the most common cause of chronic liver disease, and jaundice was the most prevalent clinical presentation (53%). There was a significant association between the liver fibrosis and MPV (P=0.025). Conclusion: MPV was significantly different between patients with different severities of liver fibrosis. However, assigning an appropriate cut off value to distinguish different degrees of fibrosis requires more studies.

scholarly journals Autophagy plays a double-edged sword role in liver diseases

2021 ◽  
Author(s):  
Jing-chao Zhou ◽  
Jing-lin Wang ◽  
Hao-zhen Ren ◽  
Xiao-lei Shi
Keyword(s):  
Liver Diseases ◽  
Alcoholic Hepatitis ◽  
Molecular Mechanisms ◽  
Membrane Vesicles ◽  
Building Blocks ◽  
Cell Types ◽  
Evolutionarily Conserved ◽  
Constitutive Process ◽  
New Strategies

Abstract As a highly evolutionarily conserved process, autophagy can be found in all types of eukaryotic cells. Such a constitutive process maintains cellular homeostasis in a wide variety of cell types through the encapsulation of damaged proteins or organelles into double-membrane vesicles. Autophagy not only simply eliminates materials but also serves as a dynamic recycling system that produces new building blocks and energy for cellular renovation and homeostasis. Previous studies have primarily recognized the role of autophagy in the degradation of dysfunctional proteins and unwanted organelles. However, there are findings of autophagy in physiological and pathological processes. In hepatocytes, autophagy is not only essential for homeostatic functions but also implicated in some diseases, such as viral hepatitis, alcoholic hepatitis, and hepatic failure. In the present review, we summarized the molecular mechanisms of autophagy and its role in several liver diseases and put forward several new strategies for the treatment of liver disease.

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