MFN1 (Mitofusin 1)

Together, our data suggest that impairment in mitochondrial dynamics of sensory neurons contributes to paclitaxel neurotoxicity and, consequently, to nociception. Therefore, preventing mitochondrial fission may be a strategy to prevent PTX-induced neurotoxicity, opening a new perspective to understanding the mechanisms involved in the development of PTX-induced neuropathy.

In vivo, MFN1-knockout NPCs exhibited reduced ECM proteoglycan levels, reinforcing its role in disc homeostasis. These findings suggest that although MFN1 and MFN2 respond to TNF-α, MFN1 reacts more robustly, making it a more promising target under inflammatory stress.

Collectively, NDUFAB1 likely promotes HCC progression by disrupting mitochondrial homeostasis, potentially through activation of the mitophagy pathway. These findings demonstrate that NDUFAB1 may be used as an independent prognostic risk factor in HCC patients.

DHYZ could improve mitochondrial dynamics and synaptic plasticity in APP/PS1 mice, inhibit oxidative stress, and thereby enhancing learning and memory abilities in APP/PS1 mice. Its mechanism might be related to activation of the cAMP/PKA/CREB-BDNF signaling pathway.

These findings offer new insights and potential targets for the preventing and treatment of cisplatin-induced ototoxicity.

Finally, MFN1 editing correlated with prolonged time to treatment and overall survival in CLL patients. Summarizing, we identified a novel ADARB1 function as C to U editing regulator, which regulates MFN1 splicing and MFN1 S329L recoding with pathogenic relevance in CLL.

High co-expression predicted poor prognosis in OSCC patients. Thus, PA28γ stabilizes C1QBP via N-terminal interaction to drive mitochondrial OXPHOS and tumor progression, highlighting its potential as a therapeutic target.

Lycopene ameliorated D-galactose-induced hepatic senescence and hepatic impairment, which may be associated with its activation of hepatic FGF21 signaling and enhancement of mitochondrial function.

LncRNA gadd7 regulated MFN1 expression by recruiting LSD1 to down-regulate H3K9me3 level and mediate mitophagy, thereby promoting AEC II apoptosis in HALI.

Mitochondrial dynamics and stability are essential for maintaining hepatic mitochondrial homeostasis and hepatocyte functions. Loss of hepatic DRP1 promotes liver tumorigenesis by increasing pyrimidine metabolism and activating the cGAS-STING-mediated innate immune response.

We characterized RAB5C (RAB5C, member RAS oncogene family) as an endosomal modulator of mitochondrial homeostasis, and SLC27A2 (solute carrier family 27 (fatty acid transporter), member 2) as a novel partner of MFN2 relevant in autophagy. We conclude that MFN proteins participate in nutrient-modulated pathways involved in organelle communication and autophagy.

Increased mitochondrial fusion in the blood of lung cancer patients may suggest an increase in protective and repair mechanisms. This opens up questions about why these mechanisms fail in the context of existing advanced cancer disease and is a starting point for further research into why protective mechanisms fail in lung cancer patients.