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Cited by 266

The DOI matches its Crossref record; 184 of the 184 references it cites were found in a registry or an index.

Role of gut microbiota and oxidative stress in the progression of non-alcoholic fatty liver disease to hepatocarcinoma: Current and innovative therapeutic approaches

Open access
Borrelli, Antonella, Bonelli, Patrizia, Tuccillo, Franca Maria, Goldfine, Ira D., Evans, Joseph L., Buonaguro, Franco Maria, Mancini, Aldo·2018·Redox Biology
DOI 10.1016/j.redox.2018.01.009
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Abstract

Non-alcoholic fatty liver disease (NAFLD) represents the most common chronic liver disease in industrialized countries. NAFLD progresses through the inflammatory phase of non-alcoholic steatohepatitis (NASH) to fibrosis and cirrhosis, with some cases developing liver failure or hepatocellular carcinoma (HCC). Liver biopsy remains the gold standard approach to a definitive diagnosis of NAFLD and the distinction between simple steatosis and NASH. The pathogenesis of NASH is still not clear. Several theories have been proposed ranging from the "Two Hit Theory" to the "Multiple Hit Theory". However, the general consensus is that the gut microbiota, oxidative stress, and mitochondrial damage play key roles in the pathogenesis of NASH. The interaction between the gut epithelia and some commensal bacteria induces the rapid generation of reactive oxygen species (ROS). The main goal of any therapy addressing NASH is to reverse or prevent progression to liver fibrosis/cirrhosis. This problem represents the first "Achilles' heel" of the new molecules being evaluated in most ongoing clinical trials. The second is the inability of these molecules to reach the mitochondria, the primary sites of energy production and ROS generation. Recently, a variety of non-pharmacological and pharmacological treatment approaches for NASH have been evaluated including vitamin E, the thiazolidinediones, and novel molecules related to NASH pathogenesis (including obeticholic acid and elafibranor). Recently, a new isoform of human manganese superoxide dismutase (MnSOD) was isolated and obtained in a synthetic recombinant form designated rMnSOD. This protein has been shown to be a powerful antioxidant capable of mediating ROS dismutation, penetrating biological barriers via its uncleaved leader peptide, and reducing portal hypertension and fibrosis in rats affected by liver cirrhosis. Based on these distinctive characteristics, it can be hypothesized that this novel recombinant protein (rMnSOD) potentially represents a new and highly efficient adjuvant therapy to counteract the progression from NASH to HCC.

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Metadata

Authors
Borrelli, A., Bonelli, P., Tuccillo, F. M., Goldfine, I. D., Evans, J. L., Buonaguro, F. M., & Mancini, A.
Venue
Redox Biology
Publisher
Elsevier BV
Published
2018-05
Volume
15
Pages
467-479
ISSN
2213-2317 (ISSN-L)
DOI
10.1016/j.redox.2018.01.009
OpenAlex
W2794269010
Cited by
266
References
184
FWCI
19.09
Type
journal article
Language
en
Open access
gold

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CoChat. (2026). Citation check: Role of gut microbiota and oxidative stress in the progression of non-alcoholic fatty liver disease to hepatocarcinoma: Current and innovative therapeutic approaches. https://app.cochat.ai/papers/10.1016/j.redox.2018.01.009
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Borrelli, A., Bonelli, P., Tuccillo, F. M., Goldfine, I. D., Evans, J. L., Buonaguro, F. M., & Mancini, A. (2018). Role of gut microbiota and oxidative stress in the progression of non-alcoholic fatty liver disease to hepatocarcinoma: Current and innovative therapeutic approaches. Redox Biology. https://doi.org/10.1016/j.redox.2018.01.009

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.