Nifedipine prevents hepatic fibrosis in a non-alcoholic steatohepatitis model induced by an L-methionine-and choline-deficient diet

Nakagami, Hironori; Shimamura, Munehisa; Miyake, Takashi; Shimosato, Takashi; Minobe, Noriko; Moritani, Toshinori; Osako, Mariana Kiomy; Nakagami, Futoshi; Kuroda, Hiroshi; Kyutoku, Mariko; Shimizu, Hideo; Katsuya, Tomohiro; Morishita, Ryuichi

doi:10.3892/mmr.2011.594

Cited by 8 publications

(1 citation statement)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is known than PPARγ plays a role in the maintenance of a quiescent HSC phenotype, and that PPARγ agonists suppress the fibrogenic potential of HSCs in vitro and in vivo ; specifically, pioglitazone and rosiglitazone, two kinds of PPARγ agonists, have been shown to alleviate liver inflammation and fibrosis in murine NASH models (Polyzos et al, 2010; Nakagami et al, 2012). Furthermore, pioglitazone also decreased liver fibrosis in patients with NASH (Gastaldelli et al, 2010; Ratziu et al, 2010); though another study reported pioglitazone could decrease inflammation in liver, but did not affect liver fibrosis (Belfort et al, 2006).…”

Section: Nuclear Receptorsmentioning

confidence: 99%

Liver Fibrogenesis in Non-Alcoholic Steatohepatitis

Bian¹,

Ma²

2012

Front. Physio.

View full text Add to dashboard Cite

Non-alcoholic fatty liver disease (NAFLD) is emerging as one of the most common chronic liver diseases in developed western countries. Non-alcoholic steatohepatitis (NASH) is the most severe form of NAFLD, and can progress to more severe forms of liver disease, including fibrosis, cirrhosis, and even hepatocellular carcinoma. The activation of hepatic stellate cells plays a critical role in NASH-related fibrogenesis. Multiple factors, such as insulin resistance, oxidative stress, pro-inflammatory cytokines and adipokines, and innate immune responses, are known to contribute to the development of NASH-related fibrogenesis. Furthermore, these factors may share synergistic interactions, which could contribute to the process of liver fibrosis. Given the complex etiology of NASH, combined treatment regimes that target these different factors provide potential treatment strategies for NASH-related liver fibrosis.

show abstract

Section: Nuclear Receptorsmentioning

confidence: 99%

Liver Fibrogenesis in Non-Alcoholic Steatohepatitis

Bian¹,

Ma²

2012

Front. Physio.

View full text Add to dashboard Cite

show abstract

Nonalcoholic Steatohepatitis: Lessons from Different Diet-induced Animal Models

Souza-Mello¹

2014

JDMDC

View full text Add to dashboard Cite

Detailed Molecular Mechanisms Involved in Drug-Induced Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis: An Update

et al. 2022

View full text Add to dashboard Cite

Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are some of the biggest public health challenges due to their spread and increasing incidence around the world. NAFLD is characterized by intrahepatic lipid deposition, accompanied by dyslipidemia, hypertension, and insulin resistance, leading to more serious complications. Among the various causes, drug administration for the treatment of numerous kinds of diseases, such as antiarrhythmic and antihypertensive drugs, promotes the onset and progression of steatosis, causing drug-induced hepatic steatosis (DIHS). Here, we reviewed in detail the major classes of drugs that cause DIHS and the specific molecular mechanisms involved in these processes. Eight classes of drugs, among the most used for the treatment of common pathologies, were considered. The most diffused mechanism whereby drugs can induce NAFLD/NASH is interfering with mitochondrial activity, inhibiting fatty acid oxidation, but other pathways involved in lipid homeostasis are also affected. PubMed research was performed to obtain significant papers published up to November 2021. The key words included the class of drugs, or the specific compound, combined with steatosis, nonalcoholic steatohepatitis, fibrosis, fatty liver and hepatic lipid deposition. Additional information was found in the citations listed in other papers, when they were not displayed in the original search.

show abstract

Nifedipine prevents hepatic fibrosis in a non-alcoholic steatohepatitis model induced by an L-methionine-and choline-deficient diet

Cited by 8 publications

References 20 publications

Liver Fibrogenesis in Non-Alcoholic Steatohepatitis

Liver Fibrogenesis in Non-Alcoholic Steatohepatitis

Nonalcoholic Steatohepatitis: Lessons from Different Diet-induced Animal Models

Detailed Molecular Mechanisms Involved in Drug-Induced Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis: An Update

Contact Info

Product

Resources

About