Metformin protects against diclofenac-induced toxicity in primary rat hepatocytes by preserving mitochondrial integrity via a pathway involving EPAC

Mora, Fabio Alejandro Aguilar; Musheshe, Nshunge; Arroyave-Ospina, Johanna C.; Geng, Yana; Soto, Juan Manuel Sánchez; Rodrigo, José A.; Alieva, Tatiana; Buist‐Homan, Manon; Lezoualc’h, Frank; Cheng, Xiaodong; Schmidt, Martina; Moshage, Han

doi:10.1016/j.biopha.2021.112072

Cited by 5 publications

(2 citation statements)

References 63 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Metformin has been proposed as a useful therapy in NAFLD and has also been reported as a potential senostatic, as discussed below. Previous results from our group have demonstrated that metformin protects against oxidative stress [200], palmitate-induced lipotoxicity [201] and diclofenac-induced liver toxicity in primary rat hepatocytes [202]. Most of these effects are related to the inhibition of mitochondrial ROS production and the preservation of mitochondrial function.…”

Section: Targeting Oxidative Stress To Modulate Cellular Senescencementioning

confidence: 94%

Modulation of Oxidative Stress-Induced Senescence during Non-Alcoholic Fatty Liver Disease

et al. 2022

Self Cite

View full text Add to dashboard Cite

Non-alcoholic fatty liver disease is characterized by disturbed lipid metabolism and increased oxidative stress. These conditions lead to the activation of different cellular response mechanisms, including senescence. Cellular senescence constitutes an important response to injury in the liver. Recent findings show that chronic oxidative stress can induce senescence, and this might be a driving mechanism for NAFLD progression, aggravating the disturbance of lipid metabolism, organelle dysfunction, pro-inflammatory response and hepatocellular damage. In this context, the modulation of cellular senescence can be beneficial to ameliorate oxidative stress-related damage during NAFLD progression. This review focuses on the role of oxidative stress and senescence in the mechanisms leading to NAFLD and discusses the possibilities to modulate senescence as a therapeutic strategy in the treatment of NAFLD.

show abstract