PKCδ modulates SP1 mediated mitochondrial autophagy to exacerbate diacetylmorphine-induced ferroptosis in neurons DOI Creative Commons

Mengjie Zhuang,

Sensen Zhu,

Liping Su

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 143, P. 113468 - 113468

Published: Oct. 28, 2024

Diacetylmorphine (DA) is widely implicated in neuronal injury; however, the underlying mechanisms remain unclear. We investigated role of iron metamorphosis DA-induced neurotoxicity using Sprague-Dawley rats and PC12 SH-SY5Y cells. Tandem mass tag proteomics analysis showed that upregulation protein kinase C delta (PKCδ) metabolism-related transferrin receptor (TFRC) significantly enriched metabolism pathway. Subsequent experiments DA exposure upregulated PKCδ cells, which increased nuclear translocation specificity 1 (SP1), intracellular free lipid peroxide levels. In addition, silencing improved behaviour restored expression level glutathione peroxidase 4 (GPX4). activated mitochondrial autophagy leading to a decrease membrane potential, accumulation reactive oxygen species (ROS), elevation LC3 (which plays key autophagy), p62 expression. Following inhibition autophagy, potential ROS were restored, as was voltage-dependent anion channel (VDAC1) GPX4. conclusion, present study suggests regulates SP1, further exacerbating ferroptosis. Therefore, or ferroptosis may be therapeutic target ameliorate following exposure.

Language: Английский

Regulating ferroptosis by non-coding RNAs in hepatocellular carcinoma DOI Creative Commons

Lijie Sun,

Hongfei Cao,

Yanzhe Wang

et al.

Biology Direct, Journal Year: 2024, Volume and Issue: 19(1)

Published: Sept. 12, 2024

Ferroptosis, a unique type of regulated cell death plays vital role in inhibiting tumour malignancy and has presented new opportunities for treatment therapy hepatocellular carcinoma. Accumulating studies indicate that epigenetic modifications by non-coding RNAs, including microRNAs, long noncoding circular can determine cancer vulnerability to ferroptosis HCC. The present review first summarize the updated core molecular mechanisms ferroptosis. We then provide concised overview modification Finally, we recent progress understanding ncRNA-mediated on will promote our regulatory modulating HCC, highlighting novel strategies HCC through targeting ncRNA-ferroptosis axis.

Language: Английский

Citations

1
The origins of light-independent magnetoreception in humans DOI Creative Commons
Takashi Shibata, Noriaki Hattori, Hisao Nishijo

et al.

Frontiers in Human Neuroscience, Journal Year: 2024, Volume and Issue: 18

Published: Nov. 29, 2024

The Earth's abundance of iron has played a crucial role in both generating its geomagnetic field and contributing to the development early life. In ancient oceans, ions, particularly around deep-sea hydrothermal vents, might have catalyzed formation macromolecules, leading emergence life Last Universal Common Ancestor. Iron continued influence catalysis, metabolism, molecular evolution, resulting creation magnetosome gene clusters magnetotactic bacteria, which enabled these unicellular organisms detect field. Although humans lack clearly identified organ for sensing, many forms adapted field-even environments-through mechanisms beyond conventional five senses. Research indicates that zebrafish hindbrains are sensitive magnetic fields, semicircular canals pigeons respond weak potential changes through electromagnetic induction, human brainwaves fields darkness. This suggests trigeminal brainstem nucleus vestibular nuclei, integrate multimodal information, play processing. From iron-based metabolic systems sensing neurons, evolution reflects ongoing adaptation However, since magnetite-activated, torque-based ion channels within cell membranes not yet been identified, specialized sensory structures like still be necessary detecting orientation. mini-review explores from light-independent magnetoreception, examining magnetite hypothesis induction as detection.

Language: Английский

Citations

1
Inorganic Nanomedicine—Mediated Ferroptosis: A Synergistic Approach to Combined Cancer Therapies and Immunotherapy DOI Open Access
Adityanarayan Mohapatra, Ayeskanta Mohanty, In‐Kyu Park

et al.

Cancers, Journal Year: 2024, Volume and Issue: 16(18), P. 3210 - 3210

Published: Sept. 20, 2024

Ferroptosis, a form of regulated cell death characterized by iron-dependent lipid peroxidation, has generated substantial interest in cancer therapy. Various methods have been developed to induce ferroptosis tumor cells, including approved drugs, experimental compounds, and nanomedicine formulations. Unlike apoptosis, presents unique molecular cellular features, representing promising approach for cancers resistant conventional treatments. Recent research indicates strong link between the immune microenvironment, suggesting potential trigger robust antitumor responses. Multiple metabolic pathways control ferroptosis, iron, lipid, redox metabolism. Thus, understanding interaction metabolism is crucial developing effective anticancer therapies. This review provides an in-depth discussion on combining inorganic nanoparticles with therapies such as phototherapy, chemotherapy, radiotherapy, immunotherapy, role these combination Furthermore, this paper explores future treatment using nanomedicine, focusing how can enhance cells boost immunity. The goal advance ferroptosis-based from laboratory clinical applications.

Language: Английский

Citations

1
Neuronal AMPK regulates lipid transport to microglia DOI

Ju-Young Bae,

Julie Jacquemyn, Maria S. Ioannou

et al.

Trends in Cell Biology, Journal Year: 2024, Volume and Issue: 34(9), P. 695 - 697

Published: Sept. 1, 2024

Language: Английский

Citations

0
Borna disease virus 1 induces ferroptosis, contributing to lethal encephalitis DOI Open Access

Tan Qing,

Hongli Yang, Yong He

et al.

Journal of Medical Virology, Journal Year: 2024, Volume and Issue: 96(10)

Published: Oct. 1, 2024

Borna disease virus 1 (BoDV-1) is a neurotropic RNA that has been linked to fatal BoDV-1 encephalitis (BVE) in humans. Ferroptosis represents newly recognized kind of programmed cell death marked by iron overload and lipid peroxidation. Various viral infections are closely related ferroptosis. However, the link between infection ferroptosis, as well its role BVE pathogenesis, remains inadequately understood. Herein, we used primary rat cortical neurons, human microglial HMC3 cells, Sprague‒Dawley rats models. induced ferroptosis characteristics were detected (iron overload, reactive oxygen species buildup, decreased antioxidant capacity, peroxidation, mitochondrial damage). Analysis via qRT-PCR Western blot demonstrated BoDV-1-induced was mediated through Nrf2/HO-1/SLC7a11/GPX4 pathway suppression. Nrf2 downregulation due promoting ubiquitination degradation. Following PTGS2/PGE2 signaling activated, various intracellular peroxidation products damage-associated molecular patterns released, contributing occurrence progression. More importantly, inhibiting or ubiquitin‒proteasome system effectively alleviated BVE. Collectively, these findings demonstrate interaction reveal an underlying pathogenic mechanism

Language: Английский

Citations

0
PKCδ modulates SP1 mediated mitochondrial autophagy to exacerbate diacetylmorphine-induced ferroptosis in neurons DOI Creative Commons

Mengjie Zhuang,

Sensen Zhu,

Liping Su

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 143, P. 113468 - 113468

Published: Oct. 28, 2024

Diacetylmorphine (DA) is widely implicated in neuronal injury; however, the underlying mechanisms remain unclear. We investigated role of iron metamorphosis DA-induced neurotoxicity using Sprague-Dawley rats and PC12 SH-SY5Y cells. Tandem mass tag proteomics analysis showed that upregulation protein kinase C delta (PKCδ) metabolism-related transferrin receptor (TFRC) significantly enriched metabolism pathway. Subsequent experiments DA exposure upregulated PKCδ cells, which increased nuclear translocation specificity 1 (SP1), intracellular free lipid peroxide levels. In addition, silencing improved behaviour restored expression level glutathione peroxidase 4 (GPX4). activated mitochondrial autophagy leading to a decrease membrane potential, accumulation reactive oxygen species (ROS), elevation LC3 (which plays key autophagy), p62 expression. Following inhibition autophagy, potential ROS were restored, as was voltage-dependent anion channel (VDAC1) GPX4. conclusion, present study suggests regulates SP1, further exacerbating ferroptosis. Therefore, or ferroptosis may be therapeutic target ameliorate following exposure.

Language: Английский

Citations

0