Rita Carini

Novara, Italy

Last Updated: 09/26/2026

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Found 15 publications

NASH-related Hepatocellular carcinoma: current therapeutic approaches and the emerging role of sodium homeostasis as a novel targeting strategy.

NASH-related Hepatocellular carcinoma: current therapeutic approaches and the emerging role of sodium homeostasis as a novel targeting strategy.

Journal: Frontiers in pharmacology

Published: July 22, 2025

Monensin Inhibits Triple-Negative Breast Cancer in Mice by a Na+-Dependent Cytotoxic Action Unrelated to Cytostatic Effects.

Monensin Inhibits Triple-Negative Breast Cancer in Mice by a Na+-Dependent Cytotoxic Action Unrelated to Cytostatic Effects.

Journal: Cells

Published: December 15, 2024

Boosting intracellular sodium selectively kills hepatocarcinoma cells and induces hepatocellular carcinoma tumor shrinkage in mice.

Boosting intracellular sodium selectively kills hepatocarcinoma cells and induces hepatocellular carcinoma tumor shrinkage in mice.

Journal: Communications biology

Published: November 29, 2022

Ischemia/Reperfusion Injury of Fatty Liver Is Protected by A2AR and Exacerbated by A1R Stimulation through Opposite Effects on ASK1 Activation.

Ischemia/Reperfusion Injury of Fatty Liver Is Protected by A2AR and Exacerbated by A1R Stimulation through Opposite Effects on ASK1 Activation.

Journal: Cells

Published: October 29, 2021

DUSP12 acts as a novel endogenous protective signal against hepatic ischemia-reperfusion damage by inhibiting ASK1 pathway.

DUSP12 acts as a novel endogenous protective signal against hepatic ischemia-reperfusion damage by inhibiting ASK1 pathway.

Journal: Clinical science (London, England : 1979)

Published: November 19, 2020

Oxidative and ER stress-dependent ASK1 activation in steatotic hepatocytes and Kupffer cells sensitizes mice fatty liver to ischemia/reperfusion injury.

Oxidative and ER stress-dependent ASK1 activation in steatotic hepatocytes and Kupffer cells sensitizes mice fatty liver to ischemia/reperfusion injury.

Journal: Free radical biology & medicine

Published: May 18, 2017

Adenosine A2a receptor stimulation blocks development of nonalcoholic steatohepatitis in mice by multilevel inhibition of signals that cause immunolipotoxicity.

Adenosine A2a receptor stimulation blocks development of nonalcoholic steatohepatitis in mice by multilevel inhibition of signals that cause immunolipotoxicity.

Journal: Translational research : the journal of laboratory and clinical medicine

Published: August 18, 2016

The balance between IL-17 and IL-22 produced by liver-infiltrating T-helper cells critically controls NASH development in mice.

The balance between IL-17 and IL-22 produced by liver-infiltrating T-helper cells critically controls NASH development in mice.

Journal: Clinical science (London, England : 1979)

Published: June 05, 2015

Pharmacological Preconditioning by Adenosine A2a Receptor Stimulation: Features of the Protected Liver Cell Phenotype.

Pharmacological Preconditioning by Adenosine A2a Receptor Stimulation: Features of the Protected Liver Cell Phenotype.

Journal: BioMed research international

Published: January 12, 2015

Mouse hepatocytes and LSEC proteome reveal novel mechanisms of ischemia/reperfusion damage and protection by A2aR stimulation.

Mouse hepatocytes and LSEC proteome reveal novel mechanisms of ischemia/reperfusion damage and protection by A2aR stimulation.

Journal: Journal of hepatology

Published: May 30, 2014

Adenosine A(2a) receptor stimulation prevents hepatocyte lipotoxicity and non-alcoholic steatohepatitis (NASH) in rats.

Adenosine A(2a) receptor stimulation prevents hepatocyte lipotoxicity and non-alcoholic steatohepatitis (NASH) in rats.

Journal: Clinical science (London, England : 1979)

Published: March 24, 2012

Role of p38 map kinase in glycine-induced hepatocyte resistance to hypoxic injury.

Role of p38 map kinase in glycine-induced hepatocyte resistance to hypoxic injury.

Journal: Journal of hepatology

Published: July 13, 2006

Showing 1-12 of 15

Last Updated: 09/26/2026