Results 51 to 60 of about 16,053 (242)

The NADPH oxidase NOX4 regulates redox and metabolic homeostasis preventing HCC progression

open access: yesHepatology, EarlyView., 2022
Loss of NOX4 in HCC tumor cells induces metabolic reprogramming in a Nrf2/MYC‐dependent manner to promote HCC progression. Abstract Background and Aims The NADPH oxidase NOX4 plays a tumor‐suppressor function in HCC. Silencing NOX4 confers higher proliferative and migratory capacity to HCC cells and increases their in vivo tumorigenic potential in ...
Irene Peñuelas‐Haro   +14 more
wiley   +1 more source

Mitochondrial stress in advanced fibrosis and cirrhosis associated with chronic hepatitis B, chronic hepatitis C, or nonalcoholic steatohepatitis

open access: yesHepatology, EarlyView., 2022
Adaptive mitochondrial mechanisms allow mitochondrial resilience and prevent the worsening of fibrosis, while deregulation of these mechanisms promotes the progression from no/minimal‐mild (F0‐F2) fibrosis to advanced fibrosis and cirrhosis (F3‐F4). Abstract Background and Aims Hepatitis B virus (HBV) infection causes oxidative stress (OS) and alters ...
Dimitri Loureiro   +17 more
wiley   +1 more source

Empagliflozin targets Mfn1 and Opa1 to attenuate microglia-mediated neuroinflammation in retinal ischemia and reperfusion injury

open access: yesJournal of Neuroinflammation, 2023
Background Neuroinflammation and mitochondrial dysfunction play crucial roles in retinal ischemia and reperfusion (IR) injury. Recent studies have identified mitochondrial function as a promising target for immunomodulation. Empagliflozin (EMPA), an anti-
Zhenlan Yang   +8 more
semanticscholar   +1 more source

5-Fluorouracil inhibits neural differentiation via Mfn1/2 reduction in human induced pluripotent stem cells

open access: diamondThe Journal of Toxicological Sciences, 2018
5-fluorouracil (5-FU) has been widely used for the treatment of tumors. Regardless of its widespread use as an anti-cancer drug, 5-FU therapy can cause several side effects, including developmental toxicity and neurotoxicity. However, the potential action of 5-FU at the early fetal stage has not yet been completely elucidated.
Shigeru Yamada   +2 more
openalex   +4 more sources

LncRNA gadd7 promotes mitochondrial membrane potential decrease and apoptosis of alveolar type II epithelial cells by positively regulating MFN1 in an in vitro model of hyperoxia-induced acute lung injury

open access: yesEuropean Journal of Histochemistry, 2023
Hyperoxia-induced acute lung injury (HALI) is a complication of oxygen therapy. LncRNA gadd7 shows associations with HALI. We explored the effects of gadd7 on mitochondrial membrane potential (MMP) and apoptosis of alveolar type II epithelial cells (AEC ...
Guoyue Liu   +5 more
semanticscholar   +1 more source

Loss of Mfn1 but not Mfn2 enhances adipogenesis

open access: green, 2022
Abstract Objective A biallelic missense mutation in mitofusin 2 ( MFN2 ) causes multiple symmetric lipomatosis and partial lipodystrophy, implicating disruption of mitochondrial fusion or interaction with other organelles in adipocyte ...
Jake P. Mann   +13 more
openalex   +2 more sources

The effects of endurance training and estrogen-related receptor α disruption on mitofusin 1 and 2, GLUT2, PPARβ/δ and SCD1 expression in the liver of diabetic rats [PDF]

open access: yesThe Ukrainian Biochemical Journal, 2020
Diabetes is a progressive and metabolic disease with a high prevalence throughout the world. Physical activity is considered as an intervention to improve diabetes. Intervention such as estrogen-related receptor α (ERRα) inhibition is considered as a new
B. Shahouzehi   +3 more
doaj   +1 more source

MFN1 deacetylation activates adaptive mitochondrial fusion and protects metabolically challenged mitochondria [PDF]

open access: yesJournal of Cell Science, 2014
Fasting and glucose shortage activate a metabolic switch that shifts more energy production to mitochondria. This metabolic adaptation ensures energy supply, but also elevates the risk of mitochondrial oxidative damage. Here we present evidence that metabolically challenged mitochondria undergo active fusion to suppress oxidative stress. In response to
Joo-Yong, Lee   +9 more
openaire   +2 more sources

Gemini-Based Lipoplexes Complement the Mitochondrial Phenotype in MFN1-Knockout Mouse Embryonic Fibroblasts [PDF]

open access: yesMolecular Pharmaceutics, 2019
Mitochondria form a dynamic network of constantly dividing and fusing organelles. The balance between these antagonistic processes is crucial for normal cellular function and requires the action of specialized proteins. The mitochondrial membrane proteins mitofusin 1 (Mfn1) and mitofusin 2 (Mfn2) are responsible for the fusion of the outer membrane of ...
Mónica Muñoz-Úbeda   +6 more
openaire   +4 more sources

Broad activation of the ubiquitin-proteasome system by Parkin is critical for mitophagy [PDF]

open access: yes, 2011
Parkin, an E3 ubiquitin ligase implicated in Parkinson's disease, promotes degradation of dysfunctional mitochondria by autophagy. Using proteomic and cellular approaches, we show that upon translocation to mitochondria, Parkin activates the ubiquitin ...
Anh H. Pham   +49 more
core   +3 more sources

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